Immuno3 0519FA Flashcards
passive immunity
acquired through PREFORMED Abs.
rapid onset.
short span of Ab (3 wks).
examples of passive immunity
IgA in breast milk.
antitoxin.
humanized monoclonal Ab.
active immunity
acquired through exposure to foreign Ags.
slow onset.
long-lasting protection (memory).
examples of active immunity
natural infx.
vaccines.
toxoid.
preformed Abs are given to pts after exposure to…?
Tetanus toxin.
Botulinum toxin.
HBV.
Rabies virus.
“To Be Healed Rapidly” with passive immunity
purpose of vaccines
induce ACTIVE immune response (humoral or cell-mediated) to specific pathogens
live attenuated vaccine
microorganism loses pathogenicity but retains capacity for transient growth within inoculated host
what kind of imm response is induced by live attenuated vaccine?
mainly cellular
pros of live attenuated vaccine
induces strong, often lifelong immunity
cons of live attenuated vaccine
may revert to VIRULENT form
examples of live attenuated vaccine
polio (Sabin).
MMR (measles, mumps, rubella).
varicella.
yellow fever.
inactivated or killed vaccine
pathogen inactivated by heat or chemicals.
maintain epitope structure of surface Ags is important for imm response.
what kind of imm response is induced by inactivated or killed vaccine?
humoral
pros of inactivated or killed vaccine
stable and safer than live vaccines
cons of inactivated or killed vaccine
weaker imm response.
BOOSTER SHOTS usually required.
examples of inactivated or killed vaccine
cholera. influenza. Hep A. polio (Salk). rabies.
autoAb: antinuclear Abs (ANA)
SLE, nonspecific
autoAb: anti-dsDNA, anti-Smith
SLE
autoAb: antihistone
drug-induced lupus
autoAb: anti-IgG (RHEUMATOID FACTOR)
RA
autoAb: anticentromere
scleroderma (CREST)
autoAb: anti-Scl-70 (anti-DNA topoisomerase I)
scleroderma (diffuse)
autoAb: antimitochondrial
primary biliary cirrhosis
autoAb: antigliadin, antiendomysial
Celiac disease
autoAb: anti-basement membrane
Goodpasture’s syndrome
autoAb: anti-desmoglein
pemphigus vulgaris
autoAb: antimicrosomal, antithyroglobulin
Hashimoto thyroiditis
autoAb: anti-Jo-1
polymyositis, dermatomyositis
autoAb: anti-SS-A (anti-Ro)
Sjogren’s syndrome
autoAb: anti-SS-B (anti-La)
Sjogren’s syndrome
autoAb: anti-U1 RNP (ribonucleoprotein)
mixed connective tissue disorder
autoAb: anti-smooth muscle
autoimmune hepatitis
autoAb: anti-glutamate decarboxylase
Type 1 diabetes mellitus
autoAb: c-ANCA
Wegener’s granulomatosis
autoAb: p-ANCA
other (non-Wegener’s) vasculitides
macrophage cytokines
IL-1 IL-6 IL-8 IL-12 TNF-a
IL-1
- endogenous pyrogen: fever, acute inflamm.
- activate endo to express adhesion molecs.
- induce chemokine secretion to recruit leukocytes.
IL-6
- endogenous pyrogen: fever.
2. stimulate production of acute phase proteins.
what cells release IL-6?
macrophages, Th2
IL-8
major chemotactic factor for neutrophils.
and induce neutrophil phagocytic activity when they arrive
IL-12
- induce differentiation of T cells into Th1 cell.
2. activate NK cells.
what cells release IL-12?
macrophages, B cells
TNF-a
“cachectin”
- septic shock
- activate endo.
- cause leuk recruitment, vasc leak.
what cytokine is secreted by all T cells?
IL-3: supports growth and differentiation of BM stem cells (acts like GM-CSF)
Th1 cytokines
IL-2
IFN-g
IL-2
stimulates growth of all T cells
IFN-g
- activate Th1 cells and macrophages (recruit leukocytes and activate phagocytosis).
- suppress Th2 cells.
- antiviral and antitumor.
Th2 cytokines
IL-4
IL-5
IL-10
IL-4
- induce differentiation into Th2 cells.
- promote growth of B cells.
- enhance class switch to IgE and IgG.
IL-5
- promote differentiation of B cells.
- enhance class switch to IgA.
- eosinophil growth and diff.
IL-10
anti-inflamm:
- inhibits action of activated T cells, Th1.
- activate Th2.
what cells secrete IL-10?
Th2 cells, regulatory T cells
what other cytokine acts like IL-10?
TGF-b: also inhibits inflamm
interferon mechanism
induce prod of RIBONUCLEASE that inhibits viral protein synth by degrading viral (not host) mRNA – places uninfected cells in an ANTIVIRAL state.
*also activate NK cells to kill virus-infected cells
what do IFN alpha and beta do?
inhibit viral protein synth
what does IFN gamma do?
increase MHC I and II expression
and Ag presentation in all cells
cell surface proteins of T cells
TCR: binds Ag-MHC complex.
CD3: assoc w/ TCR for signal transduction.
CD28: binds B7 of APC.
also…
CD4: helper T cells.
CD8: cytotoxic T cells.
cell surface proteins of B cells
Ig: binds Ag.
CD19, 20, 21, 40.
MHC II and B7: APC fx.
which B cell surface proteins is a receptor for EBV?
CD21
“you can drink Beer at the Bar when you’re 21”
cell surface proteins of macrophages
CD14, 40.
MHC II and B7.
Fc and C3b receptors: enhance phagocytosis.
cell surface proteins of NK cells
CD16: bind Fc of IgG.
CD56: unique to NK cells*
what are the ONLY mature cells in the body to NOT have MHC I?
RBCs
anergy
without costimulatory molecule, self-reactive T cells become nonreactive
*in B cells, anergy also happens but tolerance is less complete
superantigens
cross-link beta-region of TCR to MHC II on APCs = uncoordinated release of IFN-g from Th1 and subsequent release of IL-1, IL-6, TNF-a from macrophages
what microorganisms produce superantigens?
S.pyogenes
S.aureus
endotoxins (LPS)
directly stimulate macrophages by binding endotoxin receptor, CD14 (Th cells not involved)
what microorganisms produce endotoxins (LPS)?
gram negatives
Ag variation in bacteria: Salmonella
2 flagellar variants
Ag variation in bacteria: Borrelia
relapsing fever
Ag variation in bacteria: Neisseria gonorrhoeae
pilus protein
Ag variation in virus: influenza
major: antigenic shift.
minor: antigenic drift.
Ag variation in parasite: trypanosome
programmed rearrangement