Term
| Alternative Pathway(innate) |
|
Definition
C3B -> C3A + C3B.
C3B + Factors B,D -> C3 convertase
Factor P(properdin) stabilizes C3
convertase on microbes
Factors H,I. Degrade C3B
Human DAF(CD55), MCP(CD46)
dissassociate convertase
C3convertase -> C5 convertase.5-9pore
CD59 prevents MAC formation(blocksC()on humans |
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Term
| Classical Pathway(Adaptive) |
|
Definition
Activated by Antigen-Antibody binding.
IgM and IgG1 are best activators
C1q Binds to FCregions of antibody.
C1r and Cs = serine proteases
Cs cleaves and activates C4,C2: Forms
c3 convertase |
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Term
|
Definition
Lectins are proteins with sugar binding
specificity
Initiated when MBL binds mannose or
N-acetylglucosamine
Activates MBL-associated Serine
proteases(MASPs)
MASPs split C4 and C2 to form C3convertase |
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|
Term
| Control of Lectin and Classical |
|
Definition
|
|
Term
|
Definition
Produced during acute phase of
inflammatory response.
Binds to polysaccharides on some bacteria and interacts with C1
Can activate classical pathway.
C1 protein Binds CRP instead of Antibody |
|
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Term
|
Definition
Activates: granular lymphocytes, ,
transports immune complexes(C3I on RBCs)
At the least coats organism to make less infectious(blocks adherence) |
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Term
|
Definition
Release of inflmmatory mediators (Mast/basophils causes degranulation)
Recruits Neutrophils
Mediates Chemotaxis of leukocytes to infection |
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|
Term
| Hereditary ANgioneurotic Edema |
|
Definition
Mutation in C1-INH
Excessive C2(kinin)
Normally down regulates activityof
classical pathway of complement,
coagulation and kinin cascade
Without it excess inflammation occurs |
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Term
|
Definition
In NK and Cytotoxic T Cells.
Release kills target cell. |
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Term
|
Definition
Small Soluble proteins.
Induce, regulate, and coordinate the innate and adaptive immune response
Cell-Cell communication |
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Term
|
Definition
Interleukins:Cytokines produced by
leukocytes and act on other
leukocytes.Il-2Ry chain
Chemokines: Small cytokines with
chemotatic(bring in cells)
Interferons: first named for antiviral
activity |
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Term
Pleiotropy
Redundancy
Synergy
Antagonism |
|
Definition
Pleiotropy: one cytokine has different
effects on different cells
Redundancy: Two or more cytokines have
similar function
Synergy: Combined effects are greater
than the additive effect
Antagonism: Effects of one cytokine inhibit the effects of another |
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Term
| Families of receptors for cytokines |
|
Definition
Chemokines: signal via G proteins and
MAPK pathway
Interleukins:Signal Via JAK-STAT |
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Term
|
Definition
Macrophages produce Cytokines at infection Activates endothelial cells(venules)to produce selectins, ligands forintegrins and chemokines
Selectins mediate rolling of neutrophils
Integrins mediate adhesion
Chemokines activate and stimulate ] migration |
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|
Term
Types of interferons
I vs II |
|
Definition
Type 1 interferons: INF-a and INF-B
Produced by virus-infected cells that
act on surrounding cells.
Increase expresion of MHC I on
infected cells
Type 2: IFN-y
Produced by NK and TH1 cells.
Activates(enhances killing) macrophages
Increase MHC I and II on many cels
Promote production of antiviralagents
by uninfectcted cells. |
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Term
|
Definition
Tissue inflammation, high fever,
Inhibition of growth of target cells
Induction of MHC-1 and MHC-2antigens
and Fc receptor
Activation of macrophages, NKC,
Cytotoxic T lymphocytes
Induction of interferons: dsRNA. RIG-1 binds to dsRNA |
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|
Term
Proinflmmatory
vs
ANti-inflammatory cytokines |
|
Definition
Proinflam: IL-1,6, TNFa
Anti: IL10,13,TGF-B |
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Term
| Cytokines in adaptive immunity |
|
Definition
Cell mediated: IL-2(induces Cytotoxic T
cell proliferation), IFN-y
Some involved in humoral as well |
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