Immunology Flashcards
Mature T-lymphocytes have these cellular markers
CD3: signal transduction T cells
CD4, CD40L: T-helper lymphocyte marker
CD5, CD8: T-cytotoxic lymphocyte marker
CD4, CD25: Regulatory T cells
All leukocyte groups have this cellular marker
CD45
Neutrophils have this cellular marker
CD15
also Reed-Sternberg Cells in Hodgkins
NK Cells have these cellular markers
CD16 (binds Fc of IgG), CD56 (unique marker for NK)
Macrophages and epithelial cells have these cellular markers
CD14: endotoxin receptor
Macrophages become multinucleated giant cells
B-lymphocytes have this cellular marker
CD19
CD20: signal transduction B cells
CD21 (EBV receptor)
CD19 cells are completely missing in this disease
Bruton agammaglobulinemia
(no peripheral immature and mature B cells, low IgG, IgM, IgA)
–> increased susceptibility to encapsulated pyogenic bacteria like H. influenzae, Strep pneumo, Pseudomonas
Triggers neutrophils to enter site of infection, induces phagocytosis in neutrophils
IL-8
Released by macrophages, endothelial cells
Stimulates growth and proliferation of stem cells in bone marrow
IL-3
Anti-inflammatory cytokines
IL-10 –> Limits the production of pro-inflammatory cytokines gamma-interferon, IL-2, IL-3, TNF-a
Triggers vasoconstriction, vascular permeability, bronchospasm
Leukotriene C4, D4, E4
Stimulates neutrophil migration to site of inflammation
Leukotriene B4, IL-8
Mediate vasodialtion, vascular permeability
PGI2, PGD2, PGE2 (also fever)
Attracts and activates neutrophils
LTB4 (C4, D4, E4)
Things that can activate mast cells
tissue trauma; complement proteins c3a, c5a; cross-linking of IgE by Antigen
Activation of Classical complement pathway
IgG, IgM bound to Ag –> binds C1
Activation of Alternative complement pathway
Microbial products directly activate complement
Form membrane attack complex
C6-C9 –> lyse microbe by creating hole in cell membrane
Secreted by Weibel-Palade bodies
P-selectin (rolling or neutrophils)
vonWillebrand factor
Role of bradykinin
mediates vasodilation, increased vascular permeability, pain (with PGE2)
Mediators of fever
IL-1, TNF, PGE2 (raises temperature set point)
Steps + Key mediators in Neutrophil arrival and function
1) Margination (vasodilation slows blood)
2) Rolling (P/E selectin bind sialyl Lewis X)
3) Adhesion (ICAM/VCAM upreg by TNF/IL-1)
(Leukocyte Adhesion Def d/t CD18 defect)
4) Transmigration/Chemotaxis (IL-8, C5a, LtB4)
5) Phagocytosis (enhanced by opsonins IgG/C3b)
(Chediak-Higashi microtubule trafficking defect)
6) O2 dependent killing (HOCl actually kills)
(CGD oxidase defect, MPO deficiency no HOCl)
7) Resolution (neutrophils become pus, disappear)
Present in late inflammation
Macrophages
Antiinflammatory cytokines produced by macrophages
IL-10, TGF-B
Present in chronic inflammation
lymphocytes, plasma cells
Activation required for CD4 helper T cells
Extracellular Ag: MHC II –> APC
B7:CD28 –> 2nd signal
TH1 secretes IFNy –> activate macro, B class switching, inhibitory to TH2
TH2 secretes IL-4, IL-5, IL-13 –> class switching, eosinophil chemotaxis and activation
Activation required for CD8 cytotoxic T cells
Intracellular Ag: MHC I –> expressed on all nucleated cells and platelets
IL-2 from CD4/TH1 –> 2nd signal
Function of FAS (CD95)
Cytotoxic T cells express FasL, which binds FAS and activates Apoptosis (extrinsic pathway)
B cell activation
Immature B cells express IgM/IgD
Antigen binding results in maturation –> plasma cells with secretion
Epitheliod histiocytes are characteristic of
Granuloma
Main antibody in secondary response to antigen
IgG