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61 Cards in this Set
- Front
- Back
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Pasteur
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Rabies Vaccine derived from cow
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von Behring
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Serum "Antitoxins"
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KABAT
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Antibodies
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Metchnikoff (Cell immunity)
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Eating cells or phagocytes greater in immunized individuals
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Janeway
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infectious nonself vs. noninfectious self which is part of molecular recognition
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Matzinger
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Danger hypothesis
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Phagocytes originate from
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myeloid leukocytes
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NK cells originate from
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lymphoid leukocytes
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Innate immunity is immediate attack on pathogen.
Non specific way your body provides DEFENSE |
skin and mucuous membranes
Temperature low pH chemical mediators Complement Defensins Phagocytic cells (myelenoid) NK cells (lymphoid) |
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Epitope
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Molecular structure within an antigen to which an AB is made
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Classical pathway
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Ag-Ab complexes
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MB-Lectin Pathway
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Lectin binding to pathogen surfaces
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Alternative
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pathogen surface
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What activates complement system
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classical
MB-lectin Alternative |
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Complement activation causes
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inflammatory cells recruited
OPSONIZATIOn of pathogens killing of pathogens |
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Alternative pathway mechanism
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c3 spontaneous hydrolysis causes
C3 (h20) binds factor B factor D Cleavage to Ba and Bb Convertase made of c3-h20-Bb |
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What molecule is a C3 convertase
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C3b-Bb
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Adding another C3 to C3 covertase makes
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C5 convertase (C3bBb3B)
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C5 convertase
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C3b Bb 3B
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CCP is an acronym for
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Classical Complement Pathway
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CCP activated by
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Lipid A
1 IgM molecule or 2 igG molecules |
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Binding of C1q to the Ig molecule
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C1r
Cleaves and activates serine protease C1s |
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MBL of the Lectin Pathway
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Mannan binding lectin binds with high affinity mannose/fucose with correct spacing
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c1s cleaves C4 to 4a and 4b
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activate C1s4b initiates C2 to cleave
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C3 convertase in Lectin pathway
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C4b2b which cleaves more c3 to c3b
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Alternative c5 convertase is made up of
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C3b Bb 3b
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Classical C5 convertase
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C4b 2b 3b
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What is the ligand on the macrophage that binds to teh c3b of the microbial surface
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Cr1 of the macrophage
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Four functions of the complement system
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1) lysis (via pore)
2) phagocytosis 3) c3a and c5a 4) recruitment and increased vascular permeability |
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Phagocytes are only activated via
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C3b and Cr1
C5a |
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Cr1
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is one membrane receptor for complement activation fragments (c3b 4b)
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Opsonization
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signal to the phagocytes to initiate ingestion and killing
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Complement and its function in recruitment
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Cell-adhesion molecules (vCAMs and iCAMS or addressins for homing)
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Big Mac acronym
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Membrane Attack Complex
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CD59
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prevents final assembly of Big Mac at the c8 to c9 stage
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Examples of phagocytes
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Neutrophils, eosinophils, dendritic cells
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Location of tissue macrophages
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alveolar (lung)
Kupffer cells (liver) Microglia (brain) Mesangial cells (kidney) |
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What is the effector mechanism of phagocyte
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Release proteases and generate oxygen radicals
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Four non oxidative ways phagocytes directly kill
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Acidification- 3.5-4.0 pH
Antimicrobial peptides (defensins) Enzymes (lysozyme) Competitors (Lactoferrin and vitamin B12) |
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Two oxidative killing mechanisms of phagocytes
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NADPH oxidase- superoxide O2
iNos-w Nitric Oxide NO |
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Respiratory burst generated by
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NADPH oxidase
NADP donates electrons to oxygens |
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Two diseases result of phagocytic defect
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1) CGD
2) Chediak Higashi Syndrome |
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Chediak Higashi Syndromes
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phagocytes are non functional because they don't fuse with lysosomes
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CGD
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NADPH (oxidative way of killing) subunits deficiency
gp91 gp22 p67, 47, 40 |
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il6
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signal hepatocytes to make acute phase proteins (PRRs)
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If TNF alpha is released from spleen and liver into the bloodstream versus in the localized tissue?
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Systemic edema decrease blood volume, hyPOproteins
Decreased Blood volume, collapse of vessels |
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Local infection- mphages release TNF alpha that cause
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release of proteins into tissue
increase phagocyte/lymphocyte into tissue Increase in platelet adhesion to blood vessel wall. |
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TCR
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T cell ANTIGEN receptor-
can't bind directly to antigen Needs MHC |
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MHC Class II components
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Extracellular Antigen
Endolytic vesicle Peptide production in PHAGOLYSOZOME Peptide binding to MHC class II Cell surface |
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MHC Class I
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Intracellular antigen
Antigen processing to peptides occurs in Proteasome Peptide is transported into ER where it is bound by MHC class I Vesicular traffick to cell surface |
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Difference in processing between MHC Clsses is that
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Class II processed in phagolysosome
Class I is processed in the PROTEOSOME. |
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Cytotoxic T cell co receptors receptors
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alpha and beta
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T cell helpers co receptors
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4 subunits
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ANCHOR RESIDUES of MHC molecule
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identical or similar among set of peptides that bind with high affinity
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How do you regulate MHC Class II expression
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Promoter sequences that bind CIITA and Rfx
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What if you like these Txn factors that bind to promoters?
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Bare Lymphocyte Syndrome
Lymphocyte is bare because it can't present antigen that allows it to be killed |
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What cytokines regulate Class I? (Cytotoxic T cells, Intracellular antigen, proteosome)
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TNF, INF alpha, beta, gamma
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Class II cytokines for MHC
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IFN gamma
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ALLOGENIC
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foreign MHC that thymocyte TCR's have a high affinity for-
Not subject to clonal selection |
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MHC restriction
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T cell receptor is SPECIFIC for 1) peptide
2) particular MHC molecule |
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Multiple MHC isotypes and polymorphisms allow an individual ...
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larger pool of foreign peptides to present to T cells.
Increase chances of EFFECTIVE adaptive immune response. |
