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162 Cards in this Set
- Front
- Back
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What secretes IL-1?
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Macrophages
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What does IL-1 do?
(4) |
- causes acute inflammation
- induces chemokine production to recruit leukocytes - activates endothelium to express adhesion molecules - an endogenous pyrogen |
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What secretes IL-2?
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Th cells
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What does IL-2 do?
(2) |
Stimulates growth of helper and cytotoxic T cells
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What secretes IL-3?
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activated T cells
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What does IL-3 do?
(1) |
- supports the growth and differentiation of bone marrow stem cells
- has a function similar to GM-CSF |
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What secretes IL-4?
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Th2 cells
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What does IL-4 do?
(2) |
- promotes growth of B cells
- enhances class switching to IgE and IgG |
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What secretes IL-5?
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Th2 cells
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Whatd does IL-5 do?
(3) |
- promotes differentiation of B cells
- enhances class switching to IgA - stimulates production and activation of eosinophils (worms) |
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What secretes IL-6?
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Th cells and Macrophages
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What does IL-6 do?
(2) |
- stimulates production of acute-phase reactants and immunoglobulins
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What secretes IL-8?
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Macrophages
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What does IL-8 do?
(1) |
- major chemotactic factor for neutrophils
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What secretes IL-10?
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regulatory T cells
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What does IL-10 do?
(3) |
- inhibits actions of activated T cells
- inhibits Th1 cells - activates Th2 cells |
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What secretes IL-12?
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B cells and Macrophages
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What does IL-12 do?
(2) |
activates NK and Th1 cells
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What secretes y-interferon?
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Th1 cells
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What does y-interferon do?
(3) |
- stimulates macrophages
- activates Th1 cells - inhibits Th2 cells |
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What secretes TNF?
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Macrophages
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Whatd does TNF do?
(3) |
- mediates septic shock
- causes leukocytes recruitment - causes vascular leak |
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"Hot T-Bone stEAk"
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- IL-1: fever (hot)
- Il-2: stimulates T cells - IL-3: stimulates Bone marrow - IL-4: stimulates IgE productions - IL-5: stimulates IgA production |
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"Clean up on AISLE 8"
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- neutrophils are recruited by IL-8 to clear infections
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Cell surface proteins of Helper T cells?
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CD4, TCR, CD3, CD28, CD40L
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Cell surface proteins of Cytotoxic T cells?
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CD8, TCR, CD3
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Cell surface proteins of B cells?
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IgM, CD19, CD20, CD21 (receptor for EBV), CD40, MHC II, B7
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Cell surface proteins of Macrophages?
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MHC II, B7, CD40, CD1, receptors for Fc and C3b
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Cell surface proteins or NK cells?
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receptors for MHC I, CD16 (binds Fc of IgG), CD56
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Cell surface proteins of all cells except mature red cells?
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MHC I
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Complement
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- system of proteinsthat interact to play a role in:
1) Humoral immunity 2) Inflammation |
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MAC of Complement
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- Membrane Attack Complex
- defends against Gram-Negative bacteria |
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How is MAC activated?
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- CLASSIC pathway --> activated by IgG or IgM
"GM makes CLASSIC cars" - ALTERNATIVE pathway --. acvtivated by molecules on the surface of microbes (especially endotoxin) |
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What are the 2 primary opsonins in bacterial defense?
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- C3b and IgG
- C3b aids in clearance of immune complexes - "C3B -- opsonizations -- Binds Bacteria" |
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What helps prevent complement activation on self-cells? (2)
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- Decay-accelerating factor (DAF)
- deficiency leads to complement-mediated lysis of RBCs and PNH - C1 esterase inhibitor - deficiency leads to Hereditary Angiodema |
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Viral Neutralization and Complement
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C1, C2, C3, C4
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Anaphylaxis and Complement
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C3a and C5a
"Anaphylaxis -- C3A and C5A" |
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Neutrophil Chemotaxis
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C5a
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Cytolysis by MAC
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C5b-C9
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Deficiency of what leads to Hereditary Angiodema?
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- deficiency of C1 esterase inhibitor
- cannot prevent complement activation on self-cells |
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C3 deficiancy leads to?
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- Severe, recurrent pyogenic sinus and respiratory tract infections
- increased susceptibility to type III hypersensitivity reactions |
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C5-C8 deficiency leads to?
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Neisseria bacteremia
(gram-negative bacteria) |
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DAF deficiency leads to?
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- (GPI-anchored enzyme)
- complement-mediated lysis of RBCs - paroxysmal nocturnal hemoglobinuria (PNH) |
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Interferons
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- α, β, γ
- 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) - activates NK cells to kill virus-infected cells "INTERFERon INTERFERres with viruses" |
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α- and β-interferons
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- inhibit viral protein synthesis
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γ-interferons
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- increase MHC I and II expression and antigen expression in all cells
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Active Immunity
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- induced after exposure to foreign antigens
- slow onset - long-lasting protection (memory) |
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Passive Immunity
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- based on receiving preformed antibodies from another host
- rapid onset - short lifespan of antibodies (half-life = 3 weeks) - ex. IgA in breast milk |
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"To Be Healed Rapidly"
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After exposure to:
- Tetanus toxin - Botulinum toxon - HBV - Rabies virus patients are given preformed antibodies (passive immunity) |
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Antigen Variation Mechanisms
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- DNA rearrangement
- RNA segment reassortment (ie. influenza major shift) |
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Antigen Variation Classic examples:
Bacteria |
- Salmonella (2 flagellar variants)
- Borrelia (relapsing fever) - Neisseria gonorrhoeae (pilus protein) |
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Antigen Variation Classic examples:
Virus |
Influenza
- major = shift - minor = drift |
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Antigen Variation Classic examples:
Parasites |
Trypanosomes (programmed rearrangement)
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Anergy
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- self-reactive T cells become nonreactive without costimulatory molecule
- B cells also become anergic, but tolerance is less complete than in T cells |
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Granulomatous Diseases
(8) |
1. Tuberculosis
2. Fungal infections (ie. histoplasmosis) 3. Syphilis 4. Leprosy 5. Cat scratch fever 6. Sarcoidosis 7. Crohn's disease 8. Berylliosis |
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Components of a granuloma?
(4) |
- Epitheloid cell
- Giant cell - Fibroblasts - Lymphocytes |
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How are Epitheloid and Giant cells induced?
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- APC takes in and presents and antigen
- Th cell is activated by APC to make IL-2 and IFN-γ - IL-2 stimulates growth of Th cell - IFN-γ stimulates monocytes to differentiate into macrophages --> then into EPITHELOID cells --> then into GIANT cells |
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Hypersensitivities
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Type I -- anaphylactic and atopic
Type II -- antibody-mediated Type III -- immune complex, serum sickness, arthus reaction Type IV -- delayed (T cell mediated) type |
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Type I Hypersensitivity
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Anaphylactic and Atopic:
- free antigen cross-links IgE on presensitized mast cells and basophils - triggers release of vasoactive amines that act at postcapillary venules (ie. histamine) - reaction develops rapidly after antigen exposure due to preformed antibody "First and Fast" (anaphylaxis) |
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Type II Hypersensitivity
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Antibody-mediated:
- IgM and IgG bind to fixed antigen on "enemy"cell - leads to lysis (by complement) or phagocytosis - antibody and complement lead to MAC "Cy-2-toxic" |
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Type III Hypersensitivity:
Immune Complex |
Immune Complex:
- antigen-antibody (IgG) complexes activate complement - complement then attracts neutrophils - neutrophils release lysosomal enzymes "Imagine an immune complex as 3 things stuck together: antigen-antibody-complement" |
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Type III Hypersensitivity:
Serum Sickness |
Serum Sickness:
- an immune complex disease in which antibodies to the foreign proteins are produced (takes 5 days) - immune complexes form and are deposited in membranes - then they fix complement here (leads to tissue damage) - more common than Arthus reaction |
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Type III Hypersensitivity:
Arthus reaction |
Arthus reaction:
- a local subacute antibody-mediated hypersensitivity reaction - intradermal injection of antigen induces antibodies - they form antigen-antibody complexes in the skin - characterized by: edema, necrosis, and activation of complement |
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Type IV Hypersensitivity
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Delayed (T cell mediated) type:
- sensitized T lymphocyted encounter antigen and then release lymphokines - leads to macrophage activation of complement - only one that is cell mediated, therefore not transferable by serum "4th and last --> delayed" |
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Which hypersensitivity types are all antibody-mediated?
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Types I, II, and III
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Test for Type I Hypersensitivity?
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Scratch test and Radioimmunosorbent assay
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3 mechanisms of Type II Hypersensitivity?
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1. Opsonize cells or activate complement
2. Antibodies recruit neutrophils and macrophages that incite tissue damage 3. Bind to normal cellular receptors and interfere with functioning |
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Test for Type II Hypersensitivity?
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Direct and Indirect Coombs test
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Serum Sickness
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- type III immune complex disease
- most serum seickness is now caused by drugs (not serum) - Presentation: fever, uticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after antigen exposure |
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What causes the Arthus reaction?
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antigen-antibody complexes
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Test for Arthus reaction?
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Immunoflourescent staining
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4 T's of type 4 hypersensitivity
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- T lymphocytes
- Transplant rejections - TB skin tests - Touching (contact dermatitis) |
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Test for Type IV Hypersensitivity?
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Patch test (ie. PPD)
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ACID
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- Anaphylactic and Atopic --> type I
- Cytotoxic (antibody mediated) --> type II - Immune complex --> type III - Delayed (cell mediated) --> type IV |
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Type I Hypersensitivity Disorders?
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- Anaphylaxis (ie. bee sting, some food/drug allergies)
- Allergic and Atopic disorders (ie. rhinitis, hay fever, eczema, hives, asthma) |
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Type II Hypersensitivity Disorders?
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- Hemolytic anemeia
- Pernicious anemia - Idiopathic thrombocytopenic purpura - Erythroblastosis fetalis - Acute hemolytic transfusion reactions - Rheumatic fever - Goodpasture's syndrome - Bullous pemphigoid - Pemphigus vulgaris - Graves's disease - Myasthenia gravis |
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Type III Hypersensitivity Disorders?
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- SLE
- Rheumatoid arthritis - Polyarteritis nodosa - Poststreptococcal glomerulonephritis - Serum sickness - Arthus reaction (ie. swelling and inflammation following tetanus vaccine) - Hypersensitivity pheumonitis (ie. farner's lung) |
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Type IV Hypersensitivity Disorders?
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- Type I DM
- Multiple sclerosis - Guillain-Barre syndrome - Hashimoto's thyroiditis - Graft-vs-Host disease - PPD (test for M. tuberculosis) - Contact dermititis (ie. poisen ivy, nickel allergy) |
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Type I Hypersensitivity Disorders -- Presentation?
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- immediate
- anaphylactic - atopic |
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Type II Hypersensitivity Disorders -- Presentation?
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Disease tends to be specific to tissue or site where antigen is found
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Type III Hypersensitivity Disorders -- Presentation?
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Can be associated with vasculitis and systemic manifestations
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Type IV Hypersensitivity Disorders -- Presentation?
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Response is delayed and does NOT involve antibodies (vs. types I, II, and III)
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Autoantibody and Associated Disorder:
Antinuclear antibodies (ANA) |
SLE
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Autoantibody and Associated Disorder:
Anti-dsDNA, anti-Smith |
Specific for SLE
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Autoantibody and Associated Disorder:
Antihistone |
Drug-induced lupus
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Autoantibody and Associated Disorder:
Anti-IgG (rheumatoid factor) |
Rheumatoid arthritis
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Autoantibody and Associated Disorder:
Anticentromere |
Scleroderma (CREST)
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Autoantibody and Associated Disorder:
Anti-Scl-70 (anti-DNA topoisomerase I) |
Scleroderma (diffuse)
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Autoantibody and Associated Disorder:
Antimitochondrial |
Primary biliary cirrhosis
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Autoantibody and Associated Disorder:
Antigliadin, Antiendomysial |
Celiac disease
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Autoantibody and Associated Disorder:
Anti-basement membrane |
Goodpasture's syndrome
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Autoantibody and Associated Disorder:
Anti-desmoglein |
Phmphigus vulgaris
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Autoantibody and Associated Disorder:
Antimicrosomal, Antithryroglobulin |
Hashimoto's thyroiditis
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Autoantibody and Associated Disorder:
Anti-Jo-1 |
- Polymyositis
- Dermatomyositis |
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Autoantibody and Associated Disorder:
Anti-SS-A (anti-Ro) |
Sjogren's syndrome
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Autoantibody and Associated Disorder:
Anti-SS-B (anti-La) |
Sjogren's syndrome
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Autoantibody and Associated Disorder:
Anti-U1 RNP (ribonucleoprotein) |
Mixed connective tissue disease
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Autoantibody and Associated Disorder:
Anti-smooth muscle |
Autoimmune hepatitis
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Autoantibody and Associated Disorder:
Anti-glutamate decarboxylase |
Type I diabetes mellitus
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Autoantibody and Associated Disorder:
c-ANCA |
Wegener's granulomatosis
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Autoantibody and Associated Disorder:
p-ANCA |
other vasculitides
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Immune Deficiencies --> Defect
Bruton's agammaglobinemia |
- B cell immune disorder
- X-linked recessive ("increased in Boys") - defect in BTK (a tyrosine kinase gene) --> blocks B cell differentiation/maturation |
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Immune Deficiencies --> Defect
Hyper-IgM syndrome |
- B cell immune disorder
- defective CD40L on helper T cells = inability to class switch |
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Immune Deficiencies --> Defect
Selective Ig deficiency |
- B cell immune disorder
- defect in isotype switching --> deficiency in specific class of immunoglobulins |
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Immune Deficiencies --> Defect
Common variable immunodeficiency (CVID) |
- B cell immune disorder
- defect in B cell maturation - many causes |
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B-cell immune disorders?
(4) |
1. Bruton's agammaglobinemia
2. Hyper-IgM syndrome 3. Selective Ig deficiency 4. CVID |
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Immune Deficiencies --> Presentation
Bruton's agammaglobinemia |
- recurrent bacterial infections after 6 months (decreased maternal IgG)
- due to opsonization defect |
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Immune Deficiencies --> Presentation
Hyper-IgM syndrome |
- severe progenic infections early in life
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Immune Deficiencies --> Presentation
Selective Ig deficiency |
- sinus and lung infections
- milk allergies - diarrhea - Anaphylaxis on exposure to blood products with IgA |
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Immune Deficiencies --> Presentation
Common variable immunodeficiency (CVID) |
- can be acquired in 20s-30s
- increased risk of: a) autoimmune disease b) lymphoma c) sinopulmonary infections |
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Immune Deficiencies --> Labs
Bruton's agammaglobinemia |
- normal pro-B
- decreased maturation - decreased # of B cells - decreased immunoglobulins of ALL classes |
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Immune Deficiencies --> Labs
Hyper-IgM syndrome |
- increased IgM
- very decreased IgG - very decreased IgA - very decreased IgE |
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Immune Deficiencies --> Labs
Selective Ig deficiency |
- IgA deficiency most common
- failure to mature into plasma cells - decreased secretory IgA |
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Immune Deficiencies --> Labs
Common variable immunodeficiency (CVID) |
- normal # of B cells
- decreased plasma cells - decreased immunoglobulin |
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T-cell immune disorders?
(4) |
1. Thymic aplasia (DiGeorge's sundrome)
2. IL-12 receptor deficiency 3. Hyper-IgE syndrome (Job's syndrome) 4. Chronic mucocutaneous cadidiasis |
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Immune Deficiencies --> Defect
Thymic aplasia (DiGeorge's syndrome) |
- T cell immune disorder
- 22q11 deletion - failure to develop 3rd and 4th pharyngeal pouches |
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Immune Deficiencies --> Defect
IL-12 receptr deficiency |
- T cell immune disorder
- decreased Th1 response |
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Immune Deficiencies --> Defect
Hyper-IgE syndrome (Job's syndrome) |
- T cell immune disorder
- Th cells fail to produce IFN-γ --> inability of neutrophils to respond to chemotactic stimuli |
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Immune Deficiencies --> Defect
Chronic munocutaneous candidiasis |
- T cell immune disorder
- T cell dysfunction |
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Immune Deficiencies --> Presentation
Thymic aplasia (DiGeorge's syndrome) |
- tetany (hypocalcemia)
- recurrent viral/fungal infections (T cell deficiency) - congenital heart and great vessel defects |
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Immune Deficiencies --> Presentation
IL-12 receptor deficiency |
- disseminated mycobacterial infections
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Immune Deficiencies --> Presentation
Hyper-IgE syndrome (Job's syndrome) |
FATED:
- coarse Facies - cold (noninflamed) staphylococcal Abscesses - retained primary Teeth - increased IgE - Dermatologic problems (eczema) |
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Immune Deficiencies --> Presentation
Chronic mucocutaneous candidiasis |
- Candida albicans infections of the skin and mucous membranes
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Immune Deficiencies --> Labs
Thymic aplasia (DiGeorge's syndrome) |
Thymus and parathyroids fail to develop:
- decreased T cells - decreased PTH - decreased Ca2+ - absent thymic shadow on CXR |
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Immune Deficiencies --> Labs
IL-12 receptor deficiency |
- decreased IFN-γ
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Immune Deficiencies --> Labs
Hyper-IgE syndrome (Job's syndrome) |
- increased IgE
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Immune Deficiencies --> Labs
Chronic mucocutaneous candidiasis |
- N/A
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B- and T-cell immune disorders?
(3) |
1. Severe combined immunodeficiency (SCID)
2. Ataxia-telangiectasi 3. Wiskott-Aldrich syndrome |
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Phagocyte dysfunction immune disorders?
(3) |
1. Leukocyte adhesion deficiency (type I)
2. Chediak-Higashi syndrome 3. Chronic granulomatous disease |
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Immune Deficiencies --> Defect
Severe combined immunodeficiency (SCID) |
- B- and T-cell immne disorder
Several types: - defective IL-2 receptor (most common -- X-linked) - adenosine deaminase deficiency - failure to synthesize MHC II antigens |
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Immune Deficiencies --> Defect
Ataxia-telangiectasia |
- B- and T-cell immune disorder
- defect in DNA repair enzymes |
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Immune Deficiencies --> Defect
Wiskott-Aldrich syndrome |
- B- and T-cell immue disorder
- X-linked recessive efect - progressive deletion of B and T cells |
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Immune Deficiencies --> Defect
Leukocyte adhesion deficiency (typeI) |
- phagocyte dysfunction immune disorder
- defect in LFA-1 integrin (CD18) protein on phagocytes |
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Immune Deficiencies --> Defect
Chediak-Higashi syndrome |
- phagocyte dysfunction immune disorder
- autosoma recessive - defect in microtubular function with decreased phagocytosis |
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Immune Deficiencies --> Defect
Chronic granuloatous disease |
- phagocyte dysfunction immune disorder
- lack of NADPH oxidase --> a) decreased reactive oxygen species (ie. superoxide) b) absent respiratory bust in neutrophils |
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Immune Deficiencies --> Presentation
Severe combined immunodeficiency (SCID) |
- recurrent viral, bacterial, fungal, and protozoal infections due to both B- and T-cell deficiency
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Immune Deficiencies --> Presentation
Ataxia-telangiectasia |
Triad:
- cerebellar defects (ataxia) - spider angiomas (telangiectasias) - IgA defiency |
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Immune Deficiencies --> Presentation
Wiskott-Aldrich syndrome |
Triad (TIE):
- Thrombocytopenic purpura - Infections - Ezema |
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Immune Deficiencies --> Presentation
Leukocyte adhesion deficiency (type I) |
- recurrent bacterial infections
- absent pus formation - delayed separation of umbilicus |
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Immune Deficiencies --> Presentation
Chediak-Higashi syndrome |
- recurrent pyogenic infetions by staphylococci and streptococci
- partial albinism - peripheral neuropathy |
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Immune Deficiencies --> Presentation
Chronic granuloatous disease |
- increased susceptibility to catalase-positive organisms (ie. S. aureus, E. coli, and Aspergilus)
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Immune Deficiencies --> Treatment
Severe combined immunodeficiency (SCID) |
- bone marrow transplant (no allograft rejection)
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Immune Deficiencies --> Labs
Severe combined immunodeficiency (SCID) |
- decreased IL-2R = decreased T-cell activation
- increased adenine = toxic to B and T cells (decreased dNTPs, decreased DNA synthesis) |
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Immune Deficiencies --> Labs
Ataxia-telangiectasia |
- IgA deficiency
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Immune Deficiencies --> Labs
Wiskott-Aldrich syndrome |
- increased IgE
- increased IgA - decreased IgM |
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Immune Deficiencies --> Labs
Leukocyte adhesion deficiency (type I) |
- neutrophilia
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Immune Deficiencies --> Labs
Cheiad-Higashi syndrome |
- N/A
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Immune Deficiencies --> Labs
Chronic granulomatous disease |
- Negative Nitroblue tetrazolium dye reduction test
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Autograft
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From self
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Syngeneic Graft
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From identical twin or clone
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Allograft
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From nonidentical individual of same species
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Xenograft
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From different species
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Transplant Rejection:
Hyperacute Rejection |
- antibody mediated (type II)
- due to the presence of preformed antidonor antibodies in the transplant recipient - occurs within minutes after transplantation |
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Transplant Rejection:
Acute Rejection |
- cell mediated
- due to cytotoxic T cells reacting against foreign MHCs - occurs weeks after transplantatoin - reversible with immunosuppresants such as cyclosporine and OKT3 |
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Transplant Rejection:
Chronic Rejection |
- T cell and antibody mediated vascular damage (obliterative vascular fibrosis)
- occurs months to years after transplantation - irreversible - Class I-MHC(non-self) is perceived by CTLs as class I-MHC(self) presenting a non-self antigen |
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Transplant Rejection:
Graft-vs-Host Disease |
- grafted immunocompetent T cells proliferate in the irradiated immunocompromised host and reject cells with "foreign" proteins
- resulting in severe organ dysfunction - major symptoms include a maculopapular rash, jaundice, hepatosplenomegaly, and diarrhea |
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Sites of block in lymphocyte development:
SCID |
a) ADA deficiency (from lymphoid stem cell to a pro-B or pro-T cell)
b) or defective IL-2 receptor (from a pro-T cell to an immature T-cell) c) from an immature T cell to a CD4+ T cell (MHC II deficiency) |
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Sites of block in lymphocyte development:
Bruton's agammaglobulinemia |
- from a pre-B cell to an immature B-cell
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Sites of block in lymphocyte development:
DiGeorge syndrome |
- from an immature T cell to either an CD8+ T cell or a CD4+ T cells
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Sites of block in lymphocyte development:
CVID |
a) from an immature B cell to an IgM producing B cell
b) of from an immature B cell to an IgG producing B cell |
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Sites of block in lymphocyte development:
Hyper-IgM syndrome |
- from an immature B cell to an IgG producing B cell
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Sites of block in lymphocyte development:
Selective IgA deficiency |
- from an immature B cell to an IgA producing B cell
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