Immunology 7 8 - PRR, TLR, Hypersensitivity Flashcards Preview

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Flashcards in Immunology 7 8 - PRR, TLR, Hypersensitivity Deck (22):

Examples of motifs that TLRs recognize

LPS, dsRNA, cell-wall components, flagellin, CpG (humans don’t have many sequences where C comes before G, thus it is an indicator for bacteria)


Passive vs active vaccine

Passive: receive preformed ABs. mother to child (placenta or milk); deliberate AB transfer (monoclonal AB). Active: induce a response. normal infection, Controlled infection (wild-type, live attenuated, recombinant), Artificial selection (inactivated, purified components, etc.) Normal and controlled is best.


Whole cell vaccine

Inactivated or attenuated. Ex. cholera, pertussis, TB, plague.


Capsular polysaccharide vaccine

Meningitis, pneumococcal pneumonia, H influenzae B.


Toxoid vaccines

Inactivated toxin. Diphtheria, Tetanus.


Whole viral particle vaccines

Inactivated/attenuated. Influenza, MMR, Polio, rabies, yellow fever.


Viral antigens

Hep B.


DNA vaccine

Clone viral gene in a plasmid. Inject into muscle (will get transcribed in cell). Should confer resistance.


Subcomponent vaccines.

1. Protein with B and T cell epitopes. 2. Non protein: B cell only. 3. B cell epitopes joined to protein (B and T cell). 4. Minimal: 2 peptides, one for B and one for T.


Live attenuated vs inactivated

Attenuated: only one booster, humoral and cell-meditated response, but less stable and can revert. Inactive: more stable, cannot revert, but more boosters


Definition of hypersensitivity

Normal mechanisms of immune function sometimes damage host. If the damage outweighs the benefit, this is hypersensitivity


Type 1: IgE-mediated hypersensitivity

2-30 min. Ag induces cross-linkage of IgE bound to mast cells and basophils. 2nd exposure releases vasoactive mediators, causes smooth muscle contraction, permeability, vasodilation.


Type 1: signs

Systemic anaphylaxis; Localized anaphylaxis: Hay fever, Asthma, Hives, Food allergies, Eczema


Type 1: mediators and Tx.

Histamine, leukotrienes, bradykinin, prostaglandins, cytokines. Treat with epinephrine, antihistamines


Type 2: Antibody-mediated cytotoxic hypersensitivity

5-8 h. Ab directed against cell-surface antigens mediates cell destruction via complement activation or ADCC (neutrophils and macrophages can also get recruited).


Type 2: signs

Blood-transfusion reactions, Erythroblastosis fetalis, Autoimmune hemolytic anemia


Type 2: example of Rh

Rh+ baby in Rh- mother. At birth some blood mixes. Mother develops IgGs against it. Second pregnancy, some RBC fragment may cross so it triggers B cells, IgG’s can cross placenta and cause erythroblastsis fetalis. Preventable with drugs.


Type 3: Immune complex- mediated hypersensitivity

2-8 h. Ag-Ab complexes deposited in various tissues (glomeruli, blood vessels) induce complement activation and an ensuing inflammatory response. Similar to Type 2, but you can see visible lump of Ag-Ab complexes plus cells etc.


Type 3: signs etc.

Localized Arthus reaction (in skin), Generalized reactions: Serum sickness, Glomerulonephritis, Rheumatoid arthritis, Systemic lupus erythematosus


Type 4: Cell-mediated hypersensitivity

24-72 h Sensitized TDTH cells release cytokines that activate macrophages or TC cells, which mediate direct cellular damage.


Type 4: signs and example causes

Signs: Contact dermatitis, Tubercular lesions, Graft rejection. Causes: TB, Listeria, herpes, measles, poison ivy


Penicillin hypersensitivity reactions

Type 1: IgE, Urticaria, systemic anaphylaxis. Type 2: IgM, IgG, hemolytic anemia. Type 3: IgG, Serum sickness, glomerulonephritis. Type 4: T dth cells, contact dermititis