Immunology 7 8 - PRR, TLR, Hypersensitivity Flashcards Preview

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Flashcards in Immunology 7 8 - PRR, TLR, Hypersensitivity Deck (22)
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1
Q

Examples of motifs that TLRs recognize

A

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)

2
Q

Passive vs active vaccine

A

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.

3
Q

Whole cell vaccine

A

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

4
Q

Capsular polysaccharide vaccine

A

Meningitis, pneumococcal pneumonia, H influenzae B.

5
Q

Toxoid vaccines

A

Inactivated toxin. Diphtheria, Tetanus.

6
Q

Whole viral particle vaccines

A

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

7
Q

Viral antigens

A

Hep B.

8
Q

DNA vaccine

A

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

9
Q

Subcomponent vaccines.

A
  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.
10
Q

Live attenuated vs inactivated

A

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

11
Q

Definition of hypersensitivity

A

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

12
Q

Type 1: IgE-mediated hypersensitivity

A

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.

13
Q

Type 1: signs

A

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

14
Q

Type 1: mediators and Tx.

A

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

15
Q

Type 2: Antibody-mediated cytotoxic hypersensitivity

A

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

16
Q

Type 2: signs

A

Blood-transfusion reactions, Erythroblastosis fetalis, Autoimmune hemolytic anemia

17
Q

Type 2: example of Rh

A

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.

18
Q

Type 3: Immune complex- mediated hypersensitivity

A

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.

19
Q

Type 3: signs etc.

A

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

20
Q

Type 4: Cell-mediated hypersensitivity

DTH

A

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

21
Q

Type 4: signs and example causes

A

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

22
Q

Penicillin hypersensitivity reactions

A

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