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80 Cards in this Set

  • Front
  • Back
APCs
Macrophage
Dendritic cell
B cell
B-cell class switching
IL-4
IL-5
IL-6 (from Th2 cell - signal 1)
And CD40 receptor on B-cell binds CD40 ligand on T-cell
Cytotoxic T-cell activation
MHC I protein presented (1)
IL-2 from Th cell (2)
Th1 cell
Regulates cell-mediated response
Secretes Th1 cytokines: IL-2, IFN-gamma
Activates macrophage & CD8 T-cell
Inhibited by IL-10
Th2 cell
Regulate HUMORAL response
Secretes Th2 cytokines: IL-4, IL-5, IL-10
Helps B cells make anti-body (IgE>IgG)
Inhibited by IFN-gamma (from Th1 cell)
What do activated lymphocytes release?
IFN-gamma
What do activated macrophages release?
IL-1, TNF-alpha
What do cytotoxic cells contain?
Preformed proteins
-perforin - helps deliver the contents of granules into target cell
-granzyme- a serine protease, activates apoptosis inside target cell
-granulysin- antimicrobial, induces apoptosis
What's the Fab fragment?
Antigen-binding fragment
Determines idiotype: unique antigen-binding pocket; only 1 antigenic specificity expressed per B cell
What's the Fc section?
Constant
Carboxy terminal
Complement binding at CH2 (IgG + IgM only)
Carbohydrate side chains
Determines isotype (IgM, IgD)
Antibody diversity is generated by:
Four mechanisms:
1. Random "recombination" of VJ (light chain) or V(D)J (heavy chain) genes
2. Randomcombination of heavy chain with light chains.
3. Somatic hypermutation (following antigen stimulation)
4. Addition of nucleotides to DNA during "recombination" by terminal deoxynucleotidyl transferase.
Major B-cell functions
Make antibody - opsonize bacteria, neutralize viruses (IgG); activate complement (IgM, IgG); sensitize mast cells (IgE)
Allergy (type I hypersensitivity): IgE
Cytotoxic (type II) and immune complex (type III) hypersensitivity: IgG
Hyperacute organ rejection (antibody mediated).
What are the T-cell functions?
CD4 T cells help B cells make antibody and produce gamma-interferon, which activates macrophages.
CD8 T cells kill virus-infected cells directly.
Delayed cell-mediated hypersensitivity (type IV)
Acute & chronic organ rejection
Where in the thymus does positive selection occur?
Cortex
Where in the thymus does negative selection occur?
Medulla
Which cytokine stimulates Th1 and Th2 (respectively)?
IL-12 (--> Th1)
IL-4 (--> Th2)
HLA-A3
Hemachromatosis
HLA-B27
Psoriasis, Ankylosing Spondylitis, IBD, Reiter's Syndrome
HLA-B8
Grave's Disease
HLA-DR2
MS, Hay Fever, SLE, Goodpastures
HLA-DR3
DM1
HLA-DR4
R.A.; DM1
HLA-DR5
Pernicious anemia --> B12 deficiency, Hashimoto's thyroiditis
HLA-DR7
SeveN=
Steroid-responsive Nephrotic syndrome
IL-1
Endogenous pyrogen
Secreted by Macrophages
Activates Endothelium to express Adhesion molecules
Vascular permeability
--> Chemokines --> Leukocyte recruitment
IL-2
Released by T cells (Th1)
Stimulates cytotoxic and helper T-cell production
IL-3
Made by T-cells
Stimulates the growth and differentiation of Bone Marrow stem cells
Like GM-CSF
IL-4
Released by Th2 cells
Induces differentiation into Th2 cells
Stimulates B cell growth
Class switching to IgE and IgG
IL-5
Released by Th2 cells
Stimulates isotype switching --> IgA
Stimulates B-cell differentiation
Stimulates Eosinophil growth & differentiation
IL-6
Released by Macrophages
Endogenous pyrogen
Causes fever & stimulates production of acute phase proteins.
IL-8
Recruits neutrophils
Clean up on "aisle 8"
Released by macrophages
IL-10
Released by Th2 and T-reg cells
Inhibits actions of T-cells and Th1
Activates Th2
TNF-alpha
Secreted by macrophages
Mediates septic shock
Activates endothelium
Causes leukocyte recruitement
Vascular leak
Interferon-gamma
Secreted by Th1 cells
Activates macrophages & Th1
Supresses Th2 cells
Antiviral & antitumor properties
Interferon (alpha, beta, gamma)
Proteins that place uninfected cells in an ANTIVIRAL state

Induce the production of a ribonuclease that inhibits viral protein synthesis by degrading viral mRNA (but NOT host mRNA)
Alpha and Beta-interferons
Inhibit viral protein synthesis
Gamma interferons
Increase MHC I and II expresssion and antigen presentation in ALL cells
Interferons
Activate NK cells to kill virus-infected cells
Cell surface proteins: T-Cells
TCR
CD-3
CD28
Cell surface proteins: Th-cells
CD4
CD40L (binds CD40 on B-cells)
Cell surface proteins: Tc-cells
CD-8
Cell-surface proteins: B-cells
Ig (binds antigen)
CD19, CD20, CD21
CD40
MHC II
B7
Cell-surface proteins: Macrophages
MHC II, B7, CD40, CD14
Receptors for Fc and C3b
Cell-surface proteins: NK cells
Receptors for MHC I
CD-16 (finds Fc of IgG)
CD56 (UNIQUE to NK)
Anergy
Self-reactive T-cells become nonreactive without costimulatory molecule

B-cells also become anergic, but tolerance is less complete than in T-cells
What are bacterial toxins and what do they do?
Superantigens (e.g. S. pyogenes and S. aureus) cross-link the beta-region of the T-cell receptor to the MHC class II on APC's
--> uncoordinated release of IFN-gamma from Th1 cells & subsequent release of IL-1, IL-6, and TNF-alpha from macrophages

Endotoxins/LPS (gram-negative bacteria) - directly stimulate macrophages by binding to endotoxin receptor CD14; Th cells are not involved
Examples of antigen variation: bacteria
Salmonella (2 flagellar variants)
Borrelia (relapsing fever)
Neisseria gonorrhoeae (pilus protein)
Examples of antigen variation: ..
trypanosomes (programmed rearrangement)
Type I Hyper-sensitivity
First is Fast
Anaphylactic & atopic
IgE on mast cells & basophils
trigger vasoactive amines (histamine) that act on postcapillary venules
Reaction after Ag exposure, due to preformed Ab
Test: scratch test & radioummunosorbent assay
Type II Hypersensitivity
Antibody mediated - IgM, IgG b ind to fixed antigen on "enemy" cell, leading to lysis (by complement) or phagocytosis
What are the 3 mechanisms of antibody mediated (type II) hypersensitivity?
3 mechs:
1. Osponize cells or activate complement
2. Antibodies recruite neutrophils and macrophages that incite tissue damage
3. Bind to normal cellular receptors and interfere with functioning

Test: direct & indirect Coombs
Which isotypes are involved with type II h.s.?
IgM & IgG
Type III hypersensitivity
Immune complexes = IgG --> complement --> attract neutrophils --> release lysosomal enzymes

Serum sickness
Arthus reaction
Serum sickness
5 days after exposure, Ab's are formed; deposited in membranes

Fix complement --> tissue damage

More common > Arthus
Arthus reaction
Intradermal injection of antigen
--> Ab's, which form ag-ab compelxes in the SKIN
Characterized by: edema, necrosis, and complement-activation.
Serum sickness
Caused mostly by DRUGS these days. Symptoms:

Fever, urticaria, lymphadenopathy 5-10 days after antigen exposure
Type IV h.s
SENSITIZED T-cells encounter antigen --> release lymphokines

--> Macrophage activation
NO antibody involved

4 T's:

T-lymphocytes
Transplant rejections
TB skin tests
Touching (contact dermatitis)
anti-dsDNA
SLE
anti-centromere
CREST
anti-Scl-70
Scleroderma
Antihistone
Drug-induced Lupus
anti-DNA topoisomerase I
same as anti-Scl-70
Scleroderma (diffuse)
Antimitochondrial
primary biliary cirrhosis
Anti-gliadin
Celiac
Anti-BM
Goodpasture's
Anti-desmoglein
Pemphigus vulgaris
Anti-microsomal
hashiMoto's thyroiditis
anti-thryoglobulin
Hashimoto's thryoiditis
Anti-Jo-1
PolyMyositis, dermatomYositis
Anti-SS-a
Sjogren's (anti-Ro)
Anti-SSb (anti-La)
Sjogren's
Anti-U1
Mixed connective tissue disease
Anti-smooth muscle
Autoimmune hepatitis (is the liver smooth muscle?)
Anti-glutamate decarboxylase
Type I DM
c-ANCA
Wegener's
p-ANCA
other vasculitides
Type I hypersensitivity & examples
Immediate
Anaphylactic
Atopic
Examples: allergic & atopic disorders (e.g. rhinitis, hay fever, eczema, hives, asthma)
Type II
Antibody-mediated (IgM, IgG bind to fixed antigen on "enemy" cell, leading to lysis (by complement) or phagocytosis. (Cy-2-toxic: antibody + complement --> MAC).
Examples:
Hemolytic anemia
Pernicious anemia
Erythroblastic fetalis
Idiopathic Thrombocytopenic Purpura (ITP)
Acute Hemolytic Transfusion Reactions
(i.e. lots of blood stuff)
Rheumatic fever (molecular mimicry)
Goodpasture's syndrome (anti-BM antibody)
2 weird names:
Bullous pemphigous & Pemphigus vulgaris
Grave's disease (B8)
Myasthenia Gravis
Type III
Immune complex (IgG complexes activate complement --> attach to neutrophils, which release lysosomal enzymes)

Think THREE things: Antigen-Antibody-Complement

Serum sickness - immune complexes are deposited in membranes --> fix complement --> tissue damage

Arthus reaction: local, subacute, intrAdermal (immune complexes in skin)

Test: immunoflouresence test

Examples: SLE
R.A.
Polyarteritis Nodosum
Post-strep glomerulonephritis
Serum sickness (fever, urticaria, arthralgias, proteinuria, LA - usually 5-10 days after exposure to antigen)
Arthus reaction (e.g. swelling & infl. post-Tetanus vaccine)
Hypersensitivity pneumonitis (e.g. Farmer's lung)
Type IV
Delayed type H.S. - sensitized T-lymphocytes encounter antigen and then release lymphokines (leads to macrophage activation; no antibody involved)

4 T's:
-T lymphocytes
-Transplant rejections
-TB skin tests
-Touching (contact dermatitis)

Examples:
Multiple sclerosis
Type I DM
Guillan-Barre
Hashimoto's Thyroiditis
Graft-vs-Host Disease
Contact dermatitis (e.g. poison ivy, nickel allergy)