Hypersensitivity Flashcards

1
Q

TLR 4 recognizes

A

LPS (gram - bacteria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

TLR 5 recognizes

A

flagellin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What TLR’s are found on dendritic cell surface and what type of infection do they recognize?

A

Bacterial recognition TLR 4 and TLR 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

TLR 9 recognizes

A

dsRNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

TLR 3 recognizes

A

unmethylated CpG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What TLR’s are found in dendritic cell endosomes and what infection type do they recognize?

A

Viral recognition TLR 3 and TLR 9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe dendritic cell bacterial recognition process

A

Recognizes DAMP or PAMP, engulfs cell, breaks down, presents protein fragments on MHCII, recognized by CD4+ Tcells in tissue or after travel to lymph node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does a Th0 that recognizes an MHCII peptide fragment secrete?

A

IL-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

IL-2 cytokine

A

pro-proliferative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

DC produces IL-12–>Th0 differentiates to:

A

Th1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Th1 secretes

A

IFN-gamma, TNF-beta, IL-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

IFN-gamma cytokine

A

pro-inflammatory, activate macrophages/other immune cells, continues to drive more Th0 –> Th1 differentiation, blocks Th2 formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

TNF-beta cytokine

A

pro-inflammtory, activate macrophages/other immune cells (with IFN-gamma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What cytokine blocks Th2 formation?

A

IFN gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

DC produces IL-4–>Th0 differentiates to:

A

Th2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Th2 secretes

A

IL-4, IL-5, IL-10, IL-13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

IL-4 cytokine

A

Activates eosinophils/mast cells, forces class switch recomb to IgG on B cells; Drives Th2 differentiation and blocks Th1.

18
Q

IL-5 cytokine

A

Activates eosinophils/mast cells, forces class switch recomb to IgG on B cells (with IL-4)

19
Q

Which cytokine blocks Th1 formation?

A

IL-4

20
Q

IgE antibodies

A

work with eosinophils and mast cells to degranulate when it recognizes patthogens; allergic rxn component

21
Q

What DC cytokine drives Th0–>Th1?

A

IL-12

22
Q

What DC cytokine drives Th0–>Th2

A

IL-4

23
Q

Basophils are associated with which cytokine?

A

IL-4

24
Q

What Ab is associated with immediate (type 1) hypersensitvity?

A

IgE Ab produced against common foreign proteins (dust, pollen, animal danders)

25
Q

Describe IgE interaction with mast cells in Immediate Hypersensitivity:

A

Mast cell binds constant domain with its Fce receptor, variant domains free to environment, 2 IgE Abs bind allergen and cross-link to lead to mast cell degranulation via normal physiologic mechanism

26
Q

Immediate (type 1) hypersensitivity identifying features:

A

wheal and flare response to skin tests

27
Q

What Ab is associated with Antibody-Mediate (type II) hypersensitivity?

A

IgM or IgG produced against body cell surface antigens.

28
Q

Describe Ab interaction in Type II hypersensitivity:

A

IgM/IgG trigger rxn by activating complement (autoimmune hemolytic anemia) OR facilitate binding of NK cells to body cells

29
Q

Antibody-mediated (type II hypersensitivity)

A

Autoimmune disorder with inappropriate Ab recognition of body’s own cells

30
Q

What bacterial infection uses a similar mechanism to Type II hypersensitivity?

A

Streptococcus pyogenes infection (cross-reactive rxn leading to complement-mediated lysis of body cells)

31
Q

Immune complex (type III) hypersensitivity

A

Overabundance of immune complexes in circulation not cleared by macrophages

32
Q

How does type III hypersensitivity lead to destruction in the body?

A

Excess of immune complexes start to stick to blood vessel walls, leading to complement activation and damage of blood vessels

33
Q

List some disease of immune complex (type III) hypersensitivity:

A

Systemic Lupus Erythematosus (SLE), chronic glomerulonephritis, serum sickness

34
Q

Type IV hypersensitivity reaction to haptens (metal or poison ivy) stimulate the production of which cell types?

A

Th1 and Th17 (secrete excess of cytokines, cause inflammation and a response that is not directed)

35
Q

What immune cell is production of IgE dependent on during inhalant allergen rxns?

A

Th2 cells (Th1 inhibit IgE production, don’t generate immediate hypersensitivity)

36
Q

Th2 cells cause what type of hypersensitivity?

A

Type I (immediate hypersensitivity)–stimulate IgE production

37
Q

Th1 cells cause which type of hypersensitivity?

A

Type IV (along with Th17)

38
Q

Delayed-type hypersensitivity is what type?

A

Type IV

39
Q

Contact hypersensitivity

A

occurs at site of contact with allergen (ex: poison ivy); sensitization stage (1st exposure) and elicitation stage (2nd exposure to Ag)

40
Q

Tuberculin-type hypersensitivity

A

Induced by CD4 Tcell response to soluble Ags from a variety of organisms

41
Q

Granulomatous hypersensitivity

A

Chronic Th1/Th17 activation, differentiation of macs into epitheliod cells, fusion to form giant cells (granulomas) driven by TNF

42
Q

Granulomatous hypersensitivity chronic diseases

A

TB, leprosy, schistosomiasis, sarcoidosis, Chron’s disease