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314 Cards in this Set
- Front
- Back
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what mhc would process mhc cells?
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mhc 1: considered inside the cell
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NK cells are considered what kind of cells
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large, granular lymphocytes
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what kind of activity do NK cells have?
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cytotoxic activity against tumor cells and some virus infected cells
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Are NK cells part of the innate or adaptive immune system?
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innate: they do not have specific receptors for antigen
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ADCC
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antibody-dependent cell-mediated cytotoxicity
ex. ab coats antigen and NK cell has a CD16 receptor that interacts with region on AB molecule causing NK-cell cytotoxicity |
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monocytes are found where?
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in the blood
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macrophages are found where?
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in the tissue
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How do monoctyes become macrophages
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-they circulate in the blood for about 8 hours, during which time they enlarge; they then migrate into tissue and differentiate into specific tissue macrophages
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how can macrophages be activated
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-phagocytosis of antigen
-contact with receptors that sense molecules present in microbial pathogens -cytokines secreted by Th cells -mediators of the inflammatory response - |
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macrophages have what enzymes
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hydrolytic
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3 big things macrophages do
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-hydrolytic enzymes kill microbes
-secrete inflammatory mediators -increased ability to activate T cells Activated macrophages also release cytokines |
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how do Th and macrophages relate to each other
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they both help to facilitate each other's activation during the immune response
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phagosome
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-vessicle after phagocytosis
-if destroying the particle, it will bind with a lysosome to form a phagolysosome and the lysosomes hydrolytic enzymes will digest eh ingested material.....digested material will then be released via exocytosis |
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opsonin
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a molecule that binds to both antigen and phagocyte, theyreby enhancing phagocytosis
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3 granulocytes
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-basophils
-neutrophils -eosinophils |
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neutrophils
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-first on site of inflammation
-phagocytic -highest amount in serum -motile: can go from blood to tisue -granules contain hydrolytic enzymes |
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extravasation definition
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-movement of circulating neutrophils into tissues
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eosinophils
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-motile
-phagocytic -granules contain hydrolytic enzymes -useful against parasites |
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Basophils
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-non-phagocytic
-release pharmacologically active substances from their cytoplasmic granules -allergic response -contain histamine in granules -found in blood Mn: allergic to basil |
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Mast cells
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-tissue form of basophils
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Dendritic Cells
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-APC
-costimulatory signals -reactive oxygen species -cytokines |
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primary lymphoid organs
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-bone marrow
-thymus |
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medulla
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inner component of a tissue formation
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cortex
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outer compartement of a tissue formation
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location of thymus
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Above the heart
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What happens to the thymus with age?
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-with age, the size of the thymus decreases, as does the amount of T cells produced
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interstitial fluid
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via thin walls in capillaries, plasma seeps out
-the fluid that permeates all tissues and bathes all cells is called interstitial fluid |
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what happens if interstitial fluid is not returned to the circulatory system
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edema
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spleen location
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high in left abdominal cavity
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components of innate immunity
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-physical, chemical and cellular barriers
-skin and mucous membranes -acidity of stomach and specialized soluble molecules that possess antimicrobial activity -various cells |
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innate immunity specificty
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it is specific for molecular pattern associated with pathogens
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self/non self discrimination of innate vs adaptive
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innate: perfect because there are no microbe-specific patterns in host
adaptive: very good: occasional failures with self/nonself discrimination |
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major cells types of innate immunity
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Phagocytes: monocytes, macrophages, eosinophils, neutrophils
-NK cells -dendritic cells |
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major cells of adaptive immnity
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T and B cells
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is complement system innate addaptive?
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both
-can be activated by ab or my molecules that recognize PAMPS |
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3 big things complement can do
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-opsonization
-lysis by MAC -inflammation from components it releases |
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TLR
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-detect microbial products and are part of the innate immunity
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4 signs of inflammation
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-swelling
-redness -heat -pain |
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major role of chemokines
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-subgoup of cytokines
-signature activity is their capacity to act as chemoattractants (agents that cause cells to move toward higher concentrations of the agent) |
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CAMs
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cell adhesion molecules
Hold are tissues together and are used by leukocytes to interact with tissue cells |
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extravasation
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when circulating leukocytes enter inflamed tissue or peripheral lymphoid organs, the cells must adhere to andd pass between the endothelial cells lining the walls of blood vessels
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do most receptors bind more than one chemokine?
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yes
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can chemokines bind to more than one receptor?
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yes, many can bind to more than one receptor
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do leukocytes normally have access to injury area?
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no because they are found in the blood vessels
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fenstrations
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slits between blood vessel epithelium
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chemotaxis is...2 parts
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1) going out of the BV
2) Going to site in tissue |
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4 steps of leukocyte extravasation
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-inflammation causes cytokines to be released that bind to epithelium and cause several receptors to be expressed on epithelium
1) rolling, mediated by selectins -cytokines induce expression of adhesion molecules of the selectin family on endothelium wall -these E and P selectin molecules bind to mucin like cell adhesion molecules on the leukocyte membrane -process tethers the leukocyte to the endothelial cell....but the shearing force of the circulating blood detaches the cell.....selectin molecules on another endothelial cell again tether the leukocyte: process is repeated so that the cell tumbles end over end .....caled rolling 2)activation by chemoattractant stimulus -rolling slows cell enough to allow interaction between chemokines -chemokines on endothelium and chemokine receptors on leukocyte provide a degree of specificty to the recruitment of WBC's to infection site 3) arrest and adhesino, mediated by integrins binding to Ig-family members -chemokines on endothelium binding to chemokine receptors on leukocytes causes a conformation change and the clustering of integrins> leads to arrest 4)transendothelial migration -arrest allows for leukocyte to squeeze out of the blood vessel into the tissues: it does this by associating with a variety of receptors - see page 332: 13-4 |
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initially what do cytokines do in the early part of an inflammatory response
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-cytokines and other mediators act on the local endothelium, inducing expression of adhesion molecules of the selectin family
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talk about the molecules involved in T cell extravasation
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1) during an inflammatory response, cytokines act on endothelium wall creating expression of adhession molecules for selectin family that is found on leukocytes
-CD34 binds to L-selectin 2) this process causes rolling and the cell slows down -this causes chemokine found on endothelium to react with leukocyte chemokine receptor....leads to activation 3)Activation leads to conformational changes that cause change in shape and expression of LFA-a that will bind to ICAM-1 on endothelium wall 4)after arrest, cell will bind to various that allow it to pass through endothelial layer -PECAM-1 binds to PECAM-1 -CD11a/CD18 on leukocyte binds to JAM-1 on endothelium pg 336 |
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CD34
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-Mucin carbohydrate found on endothelium in the initial part of the extravasation of leukocytes
-Bind to Selectins |
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selectin
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-attached to leukocytes
-bind to mucin on endothelial cells -this binding slows cell down during the rolling phase correction......involved during early part of rolling......can be found on both leukocyte or endothelial |
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LFA-1
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-an integrin involved in naive T cell extravasation through high-endothelial venule
-binds to ICAM-1 -involved in arrest/adhesion after cells has come into contact with its chemokine |
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ICAM-1
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-Ig superfamily CAM's
-binds to LFA-1 -involved in arrest of cells |
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talk about selectin vs integrin binding
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selectin: weak
integrin: stronger |
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what does E-selectin bind to
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-E selectin is found on the endothelium....binds to mucin
***Remember selectin can be found on both leukocytes and the membrane...just as can mucin -It binds to s-Lex expressed on RBC and WBC |
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s-Lex
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-found on RBC and WBC
-Binds to E-selectin |
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E-selectin
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on endothelium
binds to s-Lex |
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chemoattractants
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1)formylated peptides
-fMet-leu-phe: bacterial proteins start with formylated peptides 2)complement anaphylotoxins: C5a, C3a 3)Chemokines -CC chemokines : aa next to eact other -CXC chemokines: spread out by 1 aa |
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MCP-1
-produced by -receptors -cells attracted -major effects |
-a CC chemokine
-monocytes, macrophages, fibroblasts, keratinocytes -CCR2B -attracted: monocytes, NK and T cells, Basophils, dendritic cells -: effect: activates macrophages, basophil histamine release |
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Eotaxin
-produced by -receptors -cells attracted -major effects |
CC chemokine
-produced by: endothelium, monocytes, epithelium, T cells -Receptors: CCR3 Cells attracted: Eosinophils, Monocytes, T cells -effect: role in allergy |
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IL-8
-produced by -receptors -cells attracted -major effects |
CXC chemokine
produced by: monocytes, macrophages, fibroblasts, keratinocytes, endothelial cells receptor: CXCR1, CXCR2 cells attracted: neutrophils, Naive T cells Effect: mobilizes, activates and degranulates neutropils, angiogenesis, acts as a neutrophil chemoattractant |
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IP-10
-produced by -receptors -cells attracted -major effects |
CXC chemokine
-produced by: keratinocytes, monocytes, T cells, fibroblasts, endohelium receptor: CXCR3 Cells attracted: Resting T cells, NK cells, Monocytes Major effect: immunostimulant, antiangiogenic, promotes TH1 immunity |
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talk about co-receptor for HIV
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-co-receptor is chemokine reeptor R4 or 5
-when chemokine binds to receptor, HIV can't bind also......HIV uses CD4 and chemokine receptor |
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does ligand always bind to same receptor?
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no
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CCR2 binds to what
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CCL2 (MCP1): is a CC subgroup of chemokines
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draw a simplified signal transduction pway for chemokine receptor
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pg 331
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CCR7
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-if found on a cell, it can be assumed that the cell is a memory T-cell
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chemokine receptors as activation markers on different cell groups:
draw groups |
page 331
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chemokine receptors are mediators of what?
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cell movement
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how do lymphocytes get back into blood?
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via the thoracic duct
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venules are what?
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-sticky, cuboidal high shape ( cells are normally flat)
-lymphocytes adhere to high endothelial venules: mediated by selectins and integrins -account for small area of endothelium -85% of bound cells adhere to these even though they only take up 1-2% of area -HEV's express several adhesion molecules -see page 335 |
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Draw scheme of lymphocyte recirculation routes:
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page 334
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define the following
selectin mucin integrin ICAMs |
selectin: membrane glycoproteins has an extracellular lectin like domain that enables the molecules to bind to specific carbohydrate groups
-has L, E and P selectin -circulating leukocytes express L-selectin -C and P selectin are expressed o vascular endothelial cells during an inflammatory response Mucin -serine and threonine rich proteins -bind to selectin -found on endothelium and leukocytes integrins: -heterodimeric with alpha and beta chain -bind to ICAMs -found on leukocyte ICAMS -Ig domain- -bind to integrins |
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what is a superfamily
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largest family with shared structure
genes and proteins are similarly organized |
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members of the Ig superfamily
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-IgG
TCR MHC CD4 and CD8 ICAM B7 Etc |
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How does endothelium become more sticky?
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-By putting P-selectin on surface
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draw 3 selectin molecules and describe their function
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lecture 14: 7c
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draw 3 leukocyte integrins
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lecute 14: 8a
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draw the breakdown of membrane phospholipid in the generation of inflammatory mediators
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pg 339
-many drugs inhibit cycloosygenase pathways and lipoxygenase pathway -prostaglandin and leukotriene A mediate inflammation |
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Draw big overall picture of inflammation from end of chapter 13
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pg 341
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is inflammation a positive or negative feedback loop?
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positive
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4 functions of cytokines
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can have
-pleiotropic -redundant -synergistic -antagonistic function |
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how can cytokines and their receptors be grouped?
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-based on common structures, subunits, and signaling machinery
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major signaling mechanism for many cytokines
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JAK/STAT system
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chemokines use what receptors to signal in what way?
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-they use serpentine (7-transmembrane) receptors to signal via trimeric G-proteins
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cytokines and chemokines allow for what?
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allow for the fine shaping and fine-tuning of an immune response as it progresses
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are cytokines soluble?
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yes....they are small proteins
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cytokines part of innate or adaptive?
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both
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cytokines mediators of what?
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-innate
-adaptive -mechanism by which leukocytes communicate with one another |
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-5 effects that cytokines can have
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-stimulation
-inhibition -differentiation -cell death -chemoattract |
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show autocrine, paracrine ad endocrine action of cytokines
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pg 303
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scheme with 5 properties of cytokines
pleiotropy....etc |
pg 304
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cytokines of innate immunity:6
cytokines of adaptive immunity:5 Secreted by? Targets and effects? |
pg 307
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local infection with gram negative bacteria vs systemic infection with gram negative bacteria
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local
-macrophage activated to secrete tnf alpha in the tissue -increased release of plasma proteins into tissue, increased phagocyte and lymphocyte migration into tissue, increased adhesion of platelet to blood vessel wall -phagocytosis of bacteria: plasma and cells drain to local lymph nodes -removal of infection and adaptive immunity systemic -macrophage activated in the liver or spleen secrete TNF alpha into the blood stream -systemic edema caused decreased blood volume, hypoproteinemia, neutropenia, followed by neutrophillia....decreased blood volume causes collapse of blood vessel -disseminated intravessicular coagulation leading to wasting and multiple organ failure -death Sepsis causes abnromal Temps, WBC counts, respiratory rate, followed by capillary leakage, tissue injury and lethal organ failure |
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virus infected host scheme
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lecture 15: 4a
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cytokine secretion and principal functions of mouse TH1 and TH2 subsets
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pg 315
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functions of cytokines in acquired immunity
-cytotoxic -TH1 -TH2 Draw what molecules would be released |
lecture 15: 4c
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IL4
IL5 IFN gamma TGF beta Role of these cytokines in regulating Ig isotype expression |
lecture 15: 5a
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5 cyokine receptors and a few members of each family
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pg 308
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draw and describe class 1 cytokine subfamilies and explain importance
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pg 309
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cytokine receptor subfamilies have what?
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shared signaling subunits
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draw IL-2R
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pg 311
-signal transduction is mediated by the beta and gamma chains, but all three chains are required for high-affinity binding of IL-2 -beta and gamma are considered a member of class 1, but alpha is not -alpha only involved in affinity for antigen -gamma chain is constitutivly expressed but beta and gamma are more expressed when exposed to antigen -this ensures that only Ag activated T cells will express the high affinity IL-2 receptor |
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talk about IL-2Ralpha
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expressed only by activated T cells: beause of this, it is sometimes referred to as the TAC (T-cell activation) antigen or CD25;
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draw pathway that class 1 and class 2 cytokine receptor signl by....
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pg 312
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JAK/STATs Used by Key cytokines
-IFN-gamma -IL-2 -IL-4 -IL-12 |
page 312
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what structure is predicted to be similar to chemokine receptor?
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retinal (when rhodopsin is bound to it)
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what kind of receptor are chemokines
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G proteins.....signal by coupling with trimeric GTP-binding proteins
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talk about IFN-g
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macrophage and NK cell activation
-associated with activation of TH1 cells -cell mediated immunity (T cell activation) -Inflammation -viruses, tuberculosis, Leishmania -Tissue immunity |
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talk about IL-4
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antibody production
-humoral immunity: Ab production -anti-inflammatory -worms, extra cellular-Bacteria, fungi, toxins, et -surface immunity |
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processing of an antigen by APC and presentation to T cell leads to what?
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-T cell activation and cytokine production
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scheme of TH1 activation, TH2, and TH17
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-ag internalized and presented by APC
-TH1 activated by release of IL-12, p40/p35>>>>>>>leads to CMI and IFN-g -APC automatically activates Th2 with presentation of Ag>>>>>>>leads to IL4 -APC activates TH17 via IL-23 and p40/p19>>>>>>>>leads to IL-17 see lecture16: 2a |
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activation of Th17 leads to what?
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-PMN-recruitment
-inflammation -IL-17 creation |
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cd40
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a co-stimulatory molecule found on APC....must bind to CD40L found on T cell to become active
-CD40L is found on CD4 cells and binds to CD40 on APC cells |
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fas ligand
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-found on CTL
-binding of fas to its receptor leads to apoptosis |
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TH1 activates what big thing
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-macrophasge
-TH1 may express Fas ligand and cause macrophage to go through apoptosis |
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TH2 activates what big thing
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-B cells
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IL-13
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secreted by TH-2 cells
important mediator of allergic inflammation and disease. |
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scheme of cytokine-mediated generation and cross-regulation of Th subsets
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pg 316
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vaccinia virus
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-member of pox virus family
-vaccine to erradicate smallpox |
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*different immune response to different pathogens: CTL, TH1 and TH2 for following
-typical pathogens -locations -antigen recognition -effector action |
cytotoxic CD8 T cell
-Typical Pathogens: Vaccinia virus, influenza virus, Rabies Virus, Listeria -Location: Cytosol -Antigen Recognition: Peptide MHC class 1 on infected cell -Effector action: killing of infected cell TH1 -pathogens: Mycobacterium tuberculosis, Mycobacterium leprae, Leishmania donovani, pneumocystis carinii ---Location: macrophage vessicle ---Ag recognition: peptide MHC class 2 on infected macrophage ---Effector action: Activation of infected macrophage TH2 -pathogens: Clostridium tetani, Staphylococcus aureus, streptococcus pneumonia, polio virus, pneumocystis carinii ---location: extracellular fluid ---Ag recognition: peptide/mhc class 2 on Ag specific B cell ---Effector: activation of specific B cell to make Ab |
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leishmania donovani
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-infects macrophage vesicles
-cleared by Th1 response -type of trypanosome protozoa -Causes Leishmaniasis from a sand flye bite -Sx of fever and skin sore from where bite occures Mn: picture a gigantic leesh on a flye infecting macrophages with a protozoa |
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listeria
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-gram positive bacteria
-infects cytosol of cells -cleared by CTL -Listeriosis symptoms include vomiting, nausea, stomach cramps, diarrhea, severe headache, constipation, persistent fever, stiff neck, loss of balance and convulsions Mn: listeria gets into your mouth cells |
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Rabies Virus
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-found in cytosol of cells
-cleared by CTL response -Sx: encephalitis (inflammation of the brain) In the beginning stages of rabies, the symptoms are malaise, headache, and fever, while in later stages it includes acute pain, violent movements, uncontrolled excitements, depressions, and the inability to swallow water (hence the name hydrophobia). In the final stages, the patient begins to have periods of mania and lethargy, and coma. Death generally occurs due to respiratory insufficiency |
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influenza virus
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-infects cytosol of cells
-cleared by CTL response |
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Pneumocystis carinii
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-pneumonia caused by yeast like fungus
-same as pneumocystis pneumonia -cleared by TH1 or TH2 response -symptoms of PCP include fever, non-productive cough, shortness of breath (especially on exertion), weight loss and night sweats. There is usually not a large amount of sputum with PCP unless the patient has an additional bacterial infection. |
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clostridium tetani
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Clostridium tetani is a rod-shaped, anaerobic bacterium of the genus Clostridium. Like other Clostridium species, it is Gram-positive
-cleared by TH2 response Mn: if you step on a nail, for positive it will hurt |
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staphylococcus pneumonia
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-gram positive
-cleared by Th2 response - |
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streptcoccus pneumonia
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-gram positive bacteria
-cleared by Th2 response |
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polio virus
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-spread via fecal oral route
-infects GI tract -can cause CNS damage leading to paralysis -cleared by TH2 response Mn: goes in hole number 2 |
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scheme of worms vs viruses and what becomes activated
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lecture 16: 3b
Viruses and some bacteria induce IL-12 secretion by dendritic cells that can activate NK cells to produce IFN-g.......... Natitive CD$ T cells activated in the presence IL-12 and IFN-g are committed to differentiate into Th1 cells Other pathogens...worms...do not induce IL-12 expression by dendritic cells but cause the synthesis and secrtion of IL-4>>>>>>>>>>>>>>Natitive CD4 T cells activated in the presence of IL-4 are committed to differentiate into TH2 cells |
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complete following for
IL-2 interferon gamma lymphotoxin IL-4 IL-5 IL-10 T-cell source, Effects on following: -b cell -t cell -macrophages -hematopoitic cells -other somatic cells -effect of gene knockout |
lecture16: 3c, 4a
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B7
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-signal 1 is generated by interaction of Ag peptide with the TCR-CD3 complex
-signal 2 is from interaction between CD28 on T cell and members of the B7 family on the APC..... -ligand for B7 can also be CTLA-4 which is an inhibitor ligand>>>>down regulation of T cells |
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Th1 response and macrophage activation scheme and what would occur
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-lecture16: 4b,c
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DTH=
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DTH=CMI
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DTH response scheme
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lecture 16: 5a
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tuberculosis is what response
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Th1
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explain Tb granuloma
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-cd-4+ TH1 cells are activated within 2-6 weeks after infection, inducing the infilitration of large numbers of activated macrophages
-These cells wall off the organism inside a granulomatous lesion called a tubercle -tubercle consists of a few small lymphocytes and a compact collection of activated macrophages, which sometimes differentiate into epithelioid cells or multinucleated giant cells pg 459 -lecture 16: 5b |
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lytic cycle results in what?
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destruction of host cell
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mycobacterium leprae tidbits
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there are 2 polar forms: several intermediates exist
tuberculoid leprosy: -organisms present at low to undetectable levels -low infectivity -granulomas and local inflammation peripheral nerve damage -normal serum immunoglobulin levles -normal T-cell response specific for M. Leprae ag -cell mediated forms granulomas -slow progression -Th1 response...with delayted type sypersensitivity: IL-2, IFN-g, TNF-B Lepromatous leprosy -organisms show florid growth in macrophages -High infectivity -disseminated infection: bone, cartilage, and diffuse nerve damage -hypergammaglobulinemia -low or absent T-cell responseiveness -no response to M. leprae antigens -Th2 response: IL-4, IL-5, IL-10 |
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leishmania lives where?
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it is an intracellular parasite that lives in macrophages phagosomes
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talk about leishmania
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-lives in macrophage phagosomes
-protozoan parasiite caused by Leishmania major -different individuals can have different Sx due to immune response -resistant individuals develop a TH1 response and clear the organism via IFN-g; non-resistant individuals develop a TH-2 response and do not clear the organism |
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talk about BALB/c and leishmania
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BALB/c mice are highly susceptible to Leishmania and frequently succumb to infection.....these mice mount a TH2 response ....they produce high levels of IL-4 and no IFN-g
-applying IL-12 to BULB C mouse makes response almost as effective as normal cells |
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what is an important source of IFN-g?
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-cytotoxic CD8 t cells
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draw TH2 respone
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lecture 16: 7b
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what response is involved in allergy?
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TH2..leads to IgE production
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schistosomiasis
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TH2 response=worm infection
Eosinophils parasitic worm -invades skin, travels to liver, reproduces -reaches maturity at 6 to 8 weeks and starts to produce eggs: eggs normally get taken from body via digestive tract, but many become trapped in the mesenteric veins, or will be washed back into the liver, where they will become lodged. -rapped eggs mature normally, secreting antigens that elicit a vigorous immune response. The eggs themselves do not damage the body. Rather it is the cellular infiltration resultant from the immune response that causes the pathology classically associated with schistosomiasis. -abdominal pain, cough, diarrhea, -worse: hepatosplenic enlargement and dermatitis |
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S. Japanicum
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type of schistomiasis
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worm infection=
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Th2 Response
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dissociation constant of receptor
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lecture 16: 9b
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NK cells fall under what group of cells
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lymphocytes
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what are the effector cells of CD8+ cells
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CTL
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Do Naive CD8+ T cells and CTL have different requirements for activation?
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yes, particularly regarding APC and costimulation
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how do CTL kill infected and tumor cells?
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by inducing apoptosis
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main effector molecules of CTL
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perforin, granzymes, granulysin......all of which are found together in lytic granules........and FasL (a surface-bound TNF family member)
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perforin
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one of main effector molecules of CTL along with granzymes, granulysin......all of which are found together in lytic granules.......and FasL......a surface-bound TNF family member
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Think what, when you see Fas
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TNF
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what happens when receptor is discovered first?
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-when receptor is discovered first, its ligand ends up getting an L after it
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Naive CD8+ T cells do not have what? and have what?
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do not have cytotoxic activity
-have a stringent requirement for costimulation |
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upon activation, naive CD8+ T cells can do what?
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differentiate into CTL: production of lytic granules, acquisition of killing activity, IFN-g secretion
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CTL have minimal or no requirement for....
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costimulation: most target cells lack B7 molecules
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co-stimulatory molecules are only presented on what?
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professional APC
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draw scheme of licensing
pg 354 |
lisensing basically primes the dendritic cell to activate cd8 cells
1)initial licencing occurs when dendritic cells interact with TH1 cells or are activated by TLR when the Ag binds to it 2)dendritic cell now shows MHC class 1 and has costimulatory molecules B7 3)Activatin of CTL-P occurs and it now bears the IL-2 receptor 4)IL-2 is released from TH1 cells and it binds to CTL-P cell causing it to become cytotoxic |
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TLR function
|
found in innate immunity
|
|
|
talk about memory CTL's
|
pg 355
antigen activated memory CTL-Ps appear to secrete sufficient IL-2 to stimulate their own proliferation and differentiation into effector CTLs.....they also may not require the CD28-B7 costimulatory signal for activation |
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what are the CTL's main weapon?
|
lytic granules....they are like smart bombs
|
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|
lytic granules are what?
|
modified lysosomes that hold effector molecules in conditions that prevent activity
|
|
|
what causes effector molecules to be released from lytic granules?
|
calcium flux induced by TCR signaling causes release of granules toward target cell
|
|
|
Once released, what do lytic granule contents do?
|
they become activated and induce programmed cell death in target cell
|
|
|
essentially what do proteases do?
|
chew up proteins to degrade them
|
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|
apoptosis in the immune system
-apoptosis= -considered what kind of cell death? -induced by what? -activation of what causes death? |
-apoptosis=programmed cell death
compartmentalized cell death: cells die without spilling contents, and express signals for rapid phagocytosis....phosphatidylserine can be induced by developmental cues, cellular damage, or signals from cytotoxic cells (CTL, NK cells) Activation of cysteine proteases, the caspases, is signal to die and also initiates cell death process |
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Features of Apoptosis....5 parts
|
-nuclear condensation
-membrane blebbing: membranes pinch off as small fragment>looks like membrane is boiling away DNA fragmentation into 200bp pieces....DNA is wrapped around histone and is degraded by proteases at 200bp intervals -degradation of cellular components -Exposure of phosphatidylserine on outer membrane leaflet: it usually only on the inner leaflet |
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is there a lot of inflammation during apoptosis?
|
no because you are not releasing fragments into the environment
|
|
|
a single differentiated CTL can do what?
|
can kill many target cells, and does not require costimulation/Th cell help
|
|
|
draw Apoptosis scheme and CTL recycling
|
pg 356
|
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proteins in lytic granules of cytotoxic T cells and Actions on target cells
|
perforin: polymerizes to form a pore in target membrane........forms large pore, allowing ions and water to flow into cell-osmotic stress induces apoptosis, but is inefficient
Granzymes: serine proteases, which activate apoptosis once in the cytoplasm of the target cell.......enter cell through perforin pore and induce apoptosis by activating caspases, initiating caspase signaling cascade Granulysin: induces apoptosis FasL: not in granules....but a mechanism for how CTL's kill -membrane-bound TNF family member, binds receptor (Fas) on target cell, activating caspase signaling cascade |
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draw CTL-mediated pore formation in target cell membrane
|
pg 358
|
|
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draw the two pathways of target-cell apoptosis stimulated by CTL's
|
pg 360
-both pathways can activate procaspase8 -UV radiation causes mitochondria to become leaky>cytochrome c released and binds to procaspase-9 -caspase 3 activation very important |
|
|
talk about specificity of apoptosis
|
-t cell recognizes infected cell
-infected cell is programmed for death -neighboring uninfected cells are not killed |
|
|
what has allowed mice to become a powerful genetic system?
|
-the ability to directly alter the genomes of mice
|
|
|
what is a transgenic mouse
|
-(Tg)
A mouse with an additional gene introduced into its genome -the gene may be wild-type (normal), mutant, or even from another species altogether -the gene is usually inserted randomly, and often as multiple tandem copies ......ex. could introduce green fluorescent gene .....many copies allows high expression levels |
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|
Knock out mouse:
|
a mouse in which a gene has been specifically inactivated by targeted deletion
---this made mice important....can not do this with fruit flyes or C. elegans |
|
|
inducible transgenic
|
can be turned off/on at will
ex. via a drug |
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|
conditional/tissue-specific knock-outs
|
only in a tissue; only in a condition
ex: want to affect liver, but not heart |
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|
knock in
|
gene inserted at specific location.......in a transgenic mouse it is inserted at a random location
|
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|
what made mice important
|
knock out mice
|
|
|
draw basic scheme for transgenic mouse
|
-563
-gene insertion is random |
|
|
Uses and caveats of Tg mice
|
uses:
-can study the function of any gene by overexpression; some by dominant negative (mutant inhibits function of normal gene) Can use RNAi technology.......transgene encodes for inhibitory RNA.... to knock down gene>>>>>>this decreases inhibition Can use tissue-specific promoters to target gene expression: Can express reporter genes (GFP, B-gal) to visualize protein expression patterns>>>>specific location Note: transgene is inherited as any dominant Mendelian trait |
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|
dominant negative
|
in Tg mice, mutant inhibits function of normal gene
|
|
|
transgene is inherited as .....
|
inherited as any dominant Mendelian trait
|
|
|
Caveats of Tg Mice
|
Lecture 17: 7c
|
|
|
2 schemes for knock-out mouse formation
|
pg 565 and 566
|
|
|
uses and caveats of KO Mice
|
lecture 17: 8c
|
|
|
talk about the 2 cool special cases of mice with: inducible transgenes and knock-in mice
|
lecture 17: 9a and b
|
|
|
draw the time course of viral infection with NK cells as the focus
|
page 361
-activity stimulated by IFN-alpha and IFN-beta -NK cells produce IFN-g that that activates macrophages>>>phagocytosis>>>>>macrophages also release IL-12>>>>>activates Th1 subset of cells |
|
|
signal transduction through TLR's-Type 1 IFN
|
lecture 18: 2a
page 70 TLR uses pway independent of MyD88 |
|
|
explain how double stranded viral RNAs can be recognized
|
lecture 18:2c
pg 63 |
|
|
draw flow diagram of a virus infected host cell
lecture 18:3a |
18: 3a
|
|
|
draw pway for induction of antiviral activity by IFN-a or b
|
pg 450
|
|
|
do NK cells express Ag specific receptors?
|
no
|
|
|
HLA=
|
HLA= MHC
human leukocyte antigen |
|
|
2 schemes of inhibitory receptor on NK cells
|
pg 363
lecture18: 3c and 4a |
|
|
what does KIR stand for?
|
killer-cell immunoglobulin-like receptors......found on NK Cells....binds to MHC class 1
|
|
|
what cells have ITIMS?
|
lecture 18: 4b
immunoreceptor tyrosin-based inhibitory motif |
|
|
sequence for ITIM and ITAM
|
lecture 18: 4c
|
|
|
ITIMS do what (easy answer)
|
antagonize ITAMS
|
|
|
other than antigen receptors, what other receptors associate with ITAM-containing chains to deliver activating signals
|
lecture 18: 5a
*remember tyrosines become phosphorylated and form docking sites for other proteins ....leads to signal |
|
|
Activating and Inhibitory Receptors.....picture with all of the receptors
other activating receptors |
lecture 18: 5b
activating receptors: NKG2D, NKp30, NKp44, 2B4, CD16 other ligands: ULPB in humans and Rae-1 in mice |
|
|
NKG2D
|
an important activating receptor that binds MIC-A and MIC-B.....these ligands are like MHC
|
|
|
other activating receptors
|
NKp30
NKp44 |
|
|
ligands are induced by.....
|
stress
|
|
|
adaptors can determine receptor status....example?
|
CD94:NKG2a------inhibitory signals
CD94:NKG2c-----activating signals |
|
|
NK cell receptors mediating activities fall into 2 structural families
|
the lectin-like receptors and the killer-cell immunoglobuline-like receptors
|
|
|
a deficiency of activating events to NK cells can lead to what?
|
-viral infection
-cancer -accumulation of damaged, non-functional cells |
|
|
genes encoding NK receptors
|
-lecture 8: pg 6a
stands for leukocyte receptor complex |
|
|
how many KIR genes are there in one organism
|
9-14
|
|
|
Talk about ligands for NKG2D
|
ligands for NKG2D are MHC-like molecules, MIC-A, MIC-B, or RAET1 family members, whose expression is induced by cellular stress
-RAET1 incudes ULBP's |
|
|
Are NK cells always cytotoxic?
|
-yes, and they always have large granules in their cytoplasm
|
|
|
NK-cell cytotoxic pathway
|
-page 360
-similar to CTL (same in the picture) |
|
|
why were NK cells named as they are?
|
-they are non-specific in their cytotoxicity
|
|
|
percent of NK cells of circulating lymphocytes
|
5-10%
|
|
|
What activates macrophages
|
IFN-g
|
|
|
NK cells are considered to be apart of innate or adaptive immunity
|
both
|
|
|
with regards to NK cell, viral infection leads to what?
|
decreased MHC class 1 expression on cells and induces NK cell killing
|
|
|
Talk about tumor cells activating NK cell
|
tumor cells have decreased MHC class 1, but increased stress-related activating NK cell ligands
|
|
|
talk about ADCC
has 2 drawings |
lecture 18: 7c and 8a
pg 366 antibody-dependent cell-mediated cytotoxicity |
|
|
NK cells are an important source of ....
|
innate IFN-g
IFN-g prevents Th2 class and forms TH1 class.....TH1 class will then form more IFN-g and NK-cells will cease |
|
|
NKT cell
|
-third type of cell identified with characteristics common to both the CTL and Nk cell
-hybrid -has TCR -do not recognize MHC-peptide complex...but a glycolipid presented *******important: releases IL-r stimulating TH2 cell lineage, and preventing TH1 lineage from forming and releasing IFN-g |
|
|
normal respiratory rate
|
20/min
|
|
|
the first line of defense against viral infections
|
NK cells
|
|
|
what leads to immunodeficiencies?
|
defects in function of immune system components
|
|
|
what are primary immunodeficiencies due to?
|
mutations in immunologically important genes
|
|
|
what are secondary immunodeficiences caused by?
|
non-genetic factors
|
|
|
Defects in each component (complement, B cells, T cells, phagocytic cells) will do what?
|
lead to specific deficiencies, based on the specific functions of the defective piece
|
|
|
SCID stands for what?
|
severe combined immunodeficiency
|
|
|
In SCID, both.........
although..... |
bot B and T cell function is impaired, although the primary deficiency may just be in the CD4+ cells
|
|
|
What does treatment of primary immunodeficiences require?
|
either bone marrow transplant or replacement/repair of the mutated gene (gene therapy)
|
|
|
primary immunodeficiency:
|
A defect in immune responses as a result of mutation in one or more immunologically important genes: inherited immunodeficiency
|
|
|
inherited immunodeficiency considered what?
|
primary immunodeficiency
|
|
|
Secondary immunodeficiency
|
impaired immune response due to extrinsic factors: acquired immunodeficiency
|
|
|
acquired immunodeficiency
|
same as secondary immunodeficiency....impaired immune response due to extrinsic factors
|
|
|
immunosuppression
|
intentional induction of immunodeficiency
|
|
|
3 parts of detecting immunodeficiency's
|
-Generally found during childhood-patients present with chronic infection, often of the same or similar type
-nature of recurrent infection gives clues as to type of immunodeficiency -Test implicated components of immune system for presence and or function |
|
|
Types of immnodeficiency (5 types)
|
lecture 19: 2b
|
|
|
flow chart of immunological defects, where they effect, and what the cause and impaired function is
|
-pg 494 and 495
|
|
|
What is complement deficiency caused by?
|
-mutation in gene for specific complement component
|
|
|
What do most complement deficiencies effect?
|
most affect complement opsonin function---this leads to susceptibility to pyogenic (pus-causing) extracellular bacteria, such as Streptococcus spp. and Staphyloccus spp. (complement required for phagocytosis
|
|
|
pyogenic
|
pus causing
|
|
|
defects in MAC component lead to what?
|
C5-C9 lead to selectie susceptibility to Neisseria spp. infections (importance of complement-mediated killing of infected cells)
|
|
|
draw flow chart of classical, lectin, and alternative pathway......what it would cause, specific components involved
|
lecture 19:3a
-immune-complex: when Ab and complement proteins bind to Ag of invader...these are then cleared by the spleen:......if not cleared they can become trapped in the kidney, lungs, skin or other tissue and lead to disease |
|
|
B cell/ antibody deficiences generally are in response to what?
|
extracellular bacteria and viruses
|
|
|
Bruton's X-linked agammaglobulinemia
|
-Btk mutation
-Block in B cell development, no peripheral B cells, no serum Ig. |
|
|
Hyper-IgM syndromes
|
defects in B cell activation and class switching-lots of IgM
littles or no IgA, IgG or IgE Caused by CD40L mutation (also some T and macrophage defects) autosomal hyper-IgM caused by mutation in AID (activation-induced cytosine deaminase)......an enzyme involved in class switching and somatic hypermutation |
|
|
selective immunoglobulin deficiencies
|
-selective IgA deficiency: unknown cause
-common variable immunodeficiency: IgM, IgG and IgA.....also called Acquired hypogammaglobulinemia -map to unkown genes in MHC locus |
|
|
T-cell deficienceis often lead to what?
|
-SCID.......increased susceptibility to all classes of pathogen
|
|
|
X-linked scid
|
-gamma constant chain defect
early block in T cell development, so no peripheral T cells |
|
|
Bare lymphocyte syndromes
|
-lead to loss of MHC molecule expression
Defects in TAP genes prevent MHC class 1 protein surface expression so no CD8+ T cells surprisingly mild immunodeficiency..... respiratory and skin infections ---Defects in TF's controlling class 2 gene expression (CIITA, RFXANK, RFX5, RFXAP) block CD4+ T cell development- result in SCID |
|
|
DiGeorge's Syndrome
|
(TBX1 deletion)....single-copy deletino of transcription factor T-Box 1, leads to defect in thymic epithelium development (similar to nude mouse).....haploinsufficiency
|
|
|
haploinsufficiency individuals can be said to be what?
|
-have Digeorge's Syndrome
|
|
|
name some B cell/ antibody deficienceis
|
bruton's X-linked agammaglobulinemia
hyper-IgM syndromes selective Ig deficiencies: selective IgA deficiency, common variable immunodeficiency |
|
|
name some T cell deficiences
|
X-linked SCID
Bare Lymphocyte Syndrome DiGeorge's Syndrome Defects in T cell signaling molecules (CD3 components, ZAP-70) defects in cytokine expression, cytokine receptors, or cytokine signaling molecules (esp. IL-7) |
|
|
CD3
|
coreceptor for TCR on T cells
|
|
|
ZAP-70
|
binds to phosphorylated CD3 leading to signal transduction pathway
|
|
|
B/T cell deficiencies.....name some
|
some forms of SCID result in lack of both B and T cells, due to mutations in genes required for development of both
ADA and PNP defects RAG1/RAG2 defects Autosomal scid Ataxia telangiectasia |
|
|
ADA and PNP defects
|
ADA (adenosine deaminase) and PNP (purine nucleotide phosphorylase) defects affect purine degradation- no B or T cells. The most common autosomal SCIDs
B/T cell deficiencies |
|
|
Most common autosomal SCIDs?
|
ADA and PNP defects
|
|
|
RAG1/RAG2 defects
|
B/T cell deficiences
recombination-activating genes proteins act synergistically and are required to mediate V-(D)-J joining |
|
|
Autosomal Scid
|
B/T cell deficiencies
(DNA repair enzyme)- defects in DNA repair enzymes lead to unrepaired double strand breaks during TCR and BCR locus rearrangement- B and T cell precursors die |
|
|
Ataxia telangiectasia
|
(ATM defect) protein involved in signaling presence of DNA double strand breaks; failure to induce DNA repair machinery during T and B cell development
|
|
|
phagocyte deficiencies lead to what
|
-phagocytic cells are crucial for immune response to bacteria and defects lead to severe susceptibility to bacterial infection
|
|
|
types of phagocyte deficiencies
|
-Severe congenital neutropenia
Cyclic neutropenia leukocyte adhesion deficiency syndrome defects in intracellular killing mechanisms (chronic granulomatous disease, G6PD deficiency, Myeloperoxidase deficiency, Chediak-Higashi syndrome) |
|
|
Chediak Higashi syndrome
|
caused by defect in lysosome-phagosome fusion
phagocyte deficiencies |
|
|
chronic granulomatous disease
|
phagocyte deficiencies
cells have trouble forming the reactive oxygen species caused by defects in NADPH oxidase system (failure to make superoxde radical) |
|
|
G6PD deficiency
|
-X linked recessive phagocyte defect
-enzyme that protects RBC's -leads to bacterial infection |
|
|
can a T cell defect affect both humoral and cell mediated parts of the immune system?
|
-yes because of its central roll in the immune system
|
|
|
pathogenic agents associated with humoral deficiency vs cell-mediated deficiency
|
humoral: extra-cellular bacteria
cell-mediated: viral, protozoan, fungal.....all intra-cellular pathogens |
|
|
definition of SCID
|
stems from defects in lymphoid development that affect T cells, either alone or in combination with B cells and NK cells
-T cell are always gone -If T and B and NK cells are gone, it becomes more serious |
|
|
Myeloperoxidase deficiency
|
Myeloperoxidase deficiency is a common genetic disorder featuring deficiency, either in quantity or function, of myeloperoxidase, an enzyme found in certain phagocytic immune cells, especially polymorphonuclear leukocytes.
phagocyte deficiency -decreased ability to kill bacteria |
|
|
neutropenis
|
reduced number of neutrophils
Severe congenital neutropenia: can be dominant or recessive....Neutrophil counts are persistently less than 0.2E9/liter (less than 10% of normal).....fatal without bone marrow transplant Cyclic neutropenia (neutrophil elastase mutation)- neutrophil numbers cycle between normal to very low/ none over 21 day period. Other hematopoitic cells have similar, but less severe, fluctuations....due to changing fluctuations of cell production via the bone marrow |
|
|
Leukocyte adhesion deficiency syndrome
|
defect in integrin common B2 subunit CD18...are required to facilitate cellular interaction
effects migration of leukocytes to area of infection causes gram-1 and gram-+ infections and fungi |
|
|
integrin family
|
functions as adhesion molecules and are required to facilitate cellular interaction
LFA-1, Mac-1 are examples have common B chain CD18 |
|
|
name the associated infectious or other diseases of the following syndromes
LAD Chronic granulomatous disease G6PD deficiency Myeloperoxidase deficiency Chediak-Higashi syndronme |
lecture 19...4c
|
|
|
other primary immunodeficiences
|
cytokine defects- mutations in IL-12, IL-12R, or IFN-γR
lead to susceptibility to otherwise non-pathogenic intracellular bacteria (esp Mycobacterium spp. and Salmonella spp.) X-linked lymphoproliferative syndrome (SAP defect) - defective control of Epstein-Barr virus (cause of mononucleosis) leads to B cell hyperproliferation, liver necrosis, and death. SAP is involved in regulating IFN-γ production by T cells in response to EBV infection. |
|
|
X-linked lymphoproliferative syndrome
|
X-linked lymphoproliferative syndrome (SAP defect) -
defective control of Epstein-Barr virus (cause of mononucleosis) leads to B cell hyperproliferation, liver necrosis, and death. SAP is involved in regulating IFN-γ production by T cells in response to EBV infection. |
|
|
treatments and problems for immunodeficiencies
|
Bone-marrow transplantation (BMT) - requires at least one
MHC allele in common between graft and patient. problem......Potential problems with bone marrow transplantation: GVHD (graft vs. host disease) - mature T cells in the bone marrow graft attack the patient’s tissues (due to alloreactivity) HVGD (host vs. graft disease) - graft is rejected by the patient’s mature T cells Gene therapy - replace defective gene in patient’s own lymphocytes or hematopoietic stem cells. Limited success with ADA gene therapy using mature lymphocytes or cord blood (HSCs). Better success with X-linked scid and retroviral transduction of bone marrow, but leukemia risk |
|
|
scheme of a bone marrow graft
|
lecture 19: 5c
|
|
|
talk about gene therapy
|
Gene therapy - replace defective gene in patient’s own
lymphocytes or hematopoietic stem cells. Limited success with ADA gene therapy using mature lymphocytes or cord blood (HSCs). Better success with X-linked scid and retroviral transduction of bone marrow, but leukemia risk |
|
|
talk about Secondary immunodeficiencies
|
Malnutrition leads to general immunosuppression, often
associated with lethal measles and tuberculosis. May be links to endocrine system (steroids, leptin) Diabetes is associated with immunosuppression Hematopoietic tumors (leukemias and lymphomas) can cause immunodeficiency due to neutrophil dysfunction or destruction of lymphoid tissues Medical interventions - chemotherapies/radiation therapy (kill bone marrow-derived cells); implanted medical devices lack innate immune responses, and serve as sites of “immune privilege” for opportunistic infections AIDS - depletion of CD4+ T cells by HIV infection |
|
|
summary of immunodeficiencies
......immune system defect with specificity and susceptible to what organism? |
lecture 19....6c
|
|
|
4 types of hyper sensitivity responses
|
372
|
|
|
general mechanism for type 1 hypersensitivity
|
373
lecture 20: 3a, 3b, 3c |
|
|
common allergens associated with type 1 hypersensitivity
|
374
|
|
|
what about house dust mite
|
fecal pellets contain Der p1 protein which people are allergic to
|
|
|
talk about the FcERI high affinity receptor
|
376
|
|
|
signal transduction pathway of mast-cell activation and degranulation
|
-378
|
|
|
kinetis of major biochemical events that follow cross-linkage of bound IgE on cultured human basophils with igE fragments
|
379
|
|
|
principal mediators involved in type 1 hypersensitivity
|
380
|
|
|
biological effects of activating mast cells and eosinophils
|
lecture 20: 5b
|
|
|
testing for an allergan
|
-Wheal and Flare Reaction
-When people undergo skin testing for allergies, allergens are rubbed onto their skin and then the skin is pricked to see if a wheal and flare reaction appears. If no reaction is observed, allergens may also be injected under the skin. Injection triggers a more intense reaction, making a wheal and flare clearly visible even if someone is only mildly allergic. A wheal and flare reaction is a skin reaction which occurs in response to exposure to an allergen. This distinctive reaction is often used in testing for allergies to determine which allergens trigger a reaction in a patient. When a wheal and flare reaction occurs outside the context of a doctor's office, it can be a sign that someone is about to experience a severe allergic reaction to something he or she has come into contact with, and it can be a good idea to be prepared for further symptoms such as difficulty breathing |
|
|
2 pictures of wheel and flare reaction
|
lecture 20: 6a and 6b
|
|
|
What is Stat6 activated in response to ?
|
IL-4......during a TH2 response
|
|
|
scheme with level of cytokine production by T cells grown in presence of IL-4
|
lecture 20: 6c
|
|
|
talk about T-bet mouse
|
lecture 20: 7a
|
|
|
talk about drugs in treating type 1
|
lecture 20: 7b
|
|
|
what type of hypersensitivity reaction would occur against blood cells?
|
type 2
|
|
|
Draw the ABO blood groups and chart with genotype, blood-group phenotype, and antigens on erythrocytes and serum antibodies
|
389
|
|
|
what kind of Ab do we make to ABO blood group antigens?
|
IgM
|
|
|
what kind of antibodies do we make to Rh factor?
|
IgG
|
|
|
development of erythroblastosis fetalis.....2 schemes
|
390
|
|
|
type 3 hypersensitivity reaction
|
called arthus reaction
lecture 20: 8c pg 392 |
|
|
talk about serum sickness
|
-immune complexes can occur which are hard for phagocytes to clear
--can cause tissue damagin type 3 reactions at various sites -complexes cause kidney probems, arthritis and vasculitis see page 392 lecture 20: 9b |
|
|
dth stands for what?
|
delayed type hypersensitivity
|
|
|
the dth response
|
-type 4
394 |
|
|
experiment showing the importance of cytokines in DTH response
|
396
|
|
|
draw contact hypersensitivity response....what type is this?
|
type 4
lecture 20: 10c 397 |
