Immune System Flashcards
IL-2
stimulates T cell growth, and activates NK cells
From T cells
IL-1
Fever
Acute inflammation, chemokine secretion
From macrophages
IL-3
Stimulates growth & differentiation of cells in BONE marrow
From T cells
IL-4
Induce Th2 differentiation & B cell growth/switching
From Th2 cells
IL-5
B cell growth & switch to IgA, & eosinophils
From Th2 cells
IL-6
Fever & acute phase proteins
From macrophages & Th2 cells
IL-10
ANTI-inflammatory!
Inhibits activated T cells & Th1 cells
From Th2 cells & Tregs
IL-8
Neutrophil chemotaxis
From macrophages
IL-12
Differentiation of T cells to Th1 cells, activate NK cells
From macrophages & B cells
TNF-alpha
Septic shock! Activates endothelium
Also insulin resistance
From macrophages
INF-gamma
*anti-viral & anti-tumor!
Activates macrophages & Th1 cells, inhibit Th2 cells
From Th1 cells
Case: Young child > 6 mo. old w/ recurrent bacterial infections, low # B cells, and low Igs of all classes.
“Bruton’s Agammaglobulinemia;” X-linked Recessive.
tyrosine kinase gene defect –> no B cell maturation
=> no opsonization
Case:
Patient has anaphylaxis to blood transfusion, also some Hx of sinopulmonary infections & chronic GI infections.
Selective IgA deficiency. *common.
LOW IgA, but normal IgM & IgG.
* anaphylaxis to transfusion bc contained IgA!
*may have false-positive beta-hCG tests (has heterophile Ab)
Case:
Age 20-30, recent increase in sinopulmonary infections. Low plasma cell on work-up.
“CVID” = Common Variable ImmunoDeficiency
(mech unknown, can be acquired as young adult)
B cell maturation defect -> normal # B cells but low plasma cells & Ig
* increased risk auto-immune disease
DiGeorge Syndrome
22q11 del. => fail to form 3rd & 4th pharyngeal arches
- tetany (hyperCa2+ bc missing parathyroids)
- recurrent fungal or viral infections (T cell def bc thymus aplasia)
- congenital heart and great vessel defects
Cause of disseminated mycobacterial infections
IL-12 deficiency –> decreased Th1 response => low IFN-gamma
Case:
Patient with…
1. Coarse Facies, 2. cold/non-inflamed staph abscesses
3. retained primary teeth, 4. eczema, 5. high IgE
Hyper-IgE syndrome/Job’s Syndrome
= failure to produce IFN-gamma => neutrophils can’t respond to chemotactic stimuli
2 causes of SCID (Severe Combined Immunodeficiency)
- defective IL-2 (X-linked Recessive)
- Adenosine DeAminase def. (AR)
=> failure to thrive bc recurrent serious infections of all kinds
* absent germinal centers & T cells
Patient presents w/ this triad:
- cerebellar defects/ataxia
- spider angiomas
- IgA deficiency
= Ataxia-Telangiectasia
(ATM gene mut –> DNA repair problem)
*increased AFP
Case: patient presents w/... 1. thrombocytopenic purpura 2. eczema 3. recurrent pyogenic infections tests show: high IgA & IgE, low IgM
Wiskott-Aldrich Syndrome (WAS mut., X-linked).
= T cells can’t recognize actin skeleton
- risk inf. by: N meningitis, H influ, Strep pneumo, PCP
Case:
Infant w/ recurrent bacterial infections but NO pus formation. Also had slow healing umbilical stump.
LAD-1 (Leukocyte Adhesion Deficiency)
= defect in LFA-1 => lymphocytes can’t migrate INTO tissues
(diapedesis blocked)
* also: neutrophilia.
Case:
Patient w/ recurrent staph & strep infections.
Other Hx: partial albino & peripheral neuropathy
Chediak-Higashi Syndrome (AR)
= Lysosomal trafficking gene mut
–> lysosome-phagosome fusion problem.
*giant granules in neutrophils
patient w/ lack of NADPH oxidase.
Disease = __?__
= Chronic Granulomatous Disease,
–> granulomatous skin lesions
*increased risk infection w/ catalase + organisms
(Staph aureus, E. coli, aspergillus)
positive selection (B & T cells)
only cells that recognize self-MHC survive
