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56 Cards in this Set
- Front
- Back
To be an effective immune system, it must: (3)
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1. Recognize and destroy a diversity of pathogens
2. Recognize effete, altered, or damaged self components 3. Exhibit tolerance to self (avoid autoimmunity) |
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2 forms of immunity
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1. Adaptive
2. Innate |
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Innate immunity characteristics (2)
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1. Provides immediate protection by direct detection of invading microbes
2. Defense response isn't any better or worse every time it sees infection |
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Adaptive Immunity (4)
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1. Adapts to a variety of non-self components
2. Responses to re-infection are faster, better and stronger 3. Develops memory though takes time to develop 4. Can anticipate all possible pathogen derived stimuli |
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What is Plasma
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Remaining stuff after cells centrifuged
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What is Serum
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Everything gone except fluid
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What attracts neutrophils to site of infection and by what process?
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chemokines by chemotaxis
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Immature form of macrophages
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monocytes
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Monocytes circulate in:
Macrophages circulate in: |
blood
tissue |
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Professional Phagocytes include (2)
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neutrophils, macrophages
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Phagocytic process:
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1. Microbe adheres to phagocyte
2. Phagocyte engulfs microbe 3. Phagosome fused with lysozome 4. Phagolysozome breaks down microbe 5. Indigestible material released by cell. |
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What does PMN stand for and give examples.
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Polymorphonuclear leukocytes
neutrophils, eosinophils, basophils |
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Mast cells are a major cause of [ ] because of [ ].
degranualte upon [ ] |
allergic symptons because of release of histamine
activation |
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Natural Killer Cells (3)
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Enter infected tissues
Kill infected cells without prior sensitization Kills cancer cells |
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Dendritic cells activate:
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naive T cells
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Dendiritic cells are [ ] [ ] [ ]
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Professional Antigen Presenting Cells
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Upon maturation which occurs during migration to secondary tissues, dendritic cells:
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dendrites become elaborated and d cells become interdigatating d.cells
facilitates extensive interaction with T cells in lymph node |
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Plasma cells are and do this:
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mature/activated B cells and secrete antibodies into the system
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B cells originate in the [ ] and migrate to the [ ] and are activated in the [ ] [ ]
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bone marrow
seconday lymph tissue/ lymph nodes germinal center |
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3 types of T Cells
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memory
Helper- encourage macrophage killing cytotoxic- kill infected target cells |
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What are PRR and what do they bind
What part of PRR bings sugar? |
Pattern recognition molecules and their CRDs (carbo recognition domains) bind terminal sugar residues found on pathogen cell walls (glucose, fucose, mannose, NOT galactose or sialic acid)
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Opsonins do what?
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coat pathogens in preparation for phagocytosis
encourages macrophage phagocytosis |
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complement activation leads to (3)
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1. Recruitment of inflammatory cells
2. Opsonization of pathogens 3. Killing of pathogens |
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classical definiton of antigen and examples
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any molecule that binds to an antibody or to T Cell receptor and is recognized by that receptor
can be foreign proteins, self proteins (altered) repetitive polymers of polysaccharides |
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portion of antigen that binds to antibody
how many areas are there on an Antigen? |
epitope
they bind with incredibly high levels of specificity (10^15) mulitple epitopes on the Ag |
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phagocyte has two receptors for opsonized pathogen. what are they?
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Fc receptor for Ab bound Ag and CR for opsonins on pathogen
together they induce phagocytosis better than alone |
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Antibodies prevent bacterial adherence to cells and activates
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complement
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Reinfection improves/retards adaptive immune response
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improves; T cells have memory for infection
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clonal selection theory is:
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T Cells that don't recognize self antigens aren't killed. Then APC presents Ag to naive T cells and T cells that match Ag become activated and proliferate and differentiate into mature T cells
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Primary Lymphoid tissue
Secondary Lymphoid tissue |
Thymus/ Bone Marrow
Lymph nodes, peyer's patches, lymphatic system, etc |
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Hematopoiesis
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Process of blood cell formation
all begin as pluripotent stem cells differentiation into different cell lines egress of cells into circulation |
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B cells/ T cells maturation differences
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B cells mature in bone marrow and circulate as mature naive cells
T cells leave bone marrow as immature thymocytes and mature in thymus |
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B Cell Development issues?
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Immature B cell has strong recognition of self antigen, either apoptosis or receptor editing for non-specificity to self antigens
*T cells undergo central tolerance in thymus |
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Lymphatic system architecture
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lymphatic capillaries in tissue space
lymphatic vessels attached to afferent vessels lymph node in between afferent and efferent vessels *act as tethers during imflammation and vasodilation |
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3 prinicipal functions of lymphatic system:
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1. collect and return interstitial fluid, including plasma proteins to blood, maintain fluid balance
2. absorb lipids from intestine and transport them to the blood 3. defend the host against infectious pathogens by enabling antigen to travel and concentrate in lymph nodes |
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T cell lymphocyte migration
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Naive travel through the blood, into secondary lymphoid tissues, then though efferent lymphatics, then back to blood.
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T/F Dendritic cells migrates to Secondary Lymphoid Tissue to present Ag to T cell
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True
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What is MHC?
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Majorhistocompatibility Complex.
a receptor that presents Ag to T cell |
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MHC molecule
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the receptor responsible for presenting peptide antigen to T cells
called Human Leukocyte Antigen in humans |
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interaction between TCR and MHC-peptide complex takes place:
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1. in the thymus during T cell selection
2. in the secondary lymphoid tissues during T cell activation 3. at the site of infection during an immune response 4. all the time during the process of immune surveillance (MHC checks all cells all the time to make sure they are self) |
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MHC class I
expression, antigen, binding, effectors, function |
all nucleated cells, professional APCs
cytoplasmic (virus) TCR of CD 8+ T cells Cytotoxic T cells Kill infected cell |
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MHC class II
expression, antigen, binding, effectors, function |
Professional APCs (only cells that can activate T cells)
Endocytic vesicles TCR of CD4+ T cells Helper T cell Help Macrophages kill Help B cells make Ab |
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MHC 1 vs MHC 2 location of pathogen
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cystolic pathogens vs endosomal or extracellular pathogens
inside vs outside |
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the breakdown of proteins and their loading is called
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antigen processing
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genetic shuffling of loops in TCR causes:
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variability in receptor specificity
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MHC 1 and 2 protein structure
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MHC 1: binds short peptides b/c MHC has pocketed off ends (longer peptides bulge out).
peptide anchored by H bonds MHC 2: binds longer peptides b/c no pockets on structure held at constant elevation above floor of MHC cleft (held up in pocket a bit) |
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MHC class 1 presentation
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protein ground up in proteasome
peptides transported by TAP into the lumen of ER peptide loaded onto MHC MHC presented on cell surface to TCR of CD8+ |
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Proteasome to Immunoproteasome
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IFN gamma induces 3 new subunits to be expressed on proteasome
3 subunits confer specificity for cleavage after hydrophobic and basic residues = peptides with prefereed binding for MHC 1 occurs during infection and allows more MHC 1 binding to T cells and activation of T cells |
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What is Tapasin
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brings MHC close to TAP proteins and exchanges suboptimal peptides for optimal peptides
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MHC class 2 presentation
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endocytosed antigens brought to ER and loaded onto MHC peoptide.
complex migrates to cell surface **endocytosis required for presentation** |
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MHC class 2 presentation more detailed
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RER synthesize MHC 2 bings to invariant chain
bound chain prevents premature binding of peptides to MHC Digestion of invariant chain leaves CLIP bound groove to MHC groove HLA-DM takes out CLIP fragment exchanges peptide from pathogen peptides can bind to MCH 2 |
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Cross presentation
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particle bigger than cell injested and ER membrane recruited to help engulf.
SEC 61 breaks down particle and feeds proteins to proteasome peptides re-enter ER with help of TAP internal peptides bind to MHC 2 and/or MHC 1 |
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3 CDRs on Vh and Vl regions (Valpha and Vbeta in TCR)
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CDR 1 2 and 3
same as hypervariable regions |
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hypervariable regions (CDRs) placement
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lie in discrete loops of the folded structure (Ab or TCR)
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Effector functions determined by
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constant regions
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dimerization of IgE following Allergan binding releases
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histamine from mast cell
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