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GI Exam #1 > Gut Immunology > Flashcards

Gut Immunology Flashcards

1
Q

Homeostasis in gut mucosa is preserved by (2)

A

Secretory IgA and induced oral tolerance.

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2
Q

How do Peyer’s patches and isolated lymphoid tissues receive Ags?

A

From Ag-transporting DCs. This is because PPs and ILFs do not have afferent lymphatics.

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3
Q

MAMPs

A

Patterns on microbes that bind to PRRs on epithelial cells and DCs.

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4
Q

Isolated lymphoid tissues

A

Single B cell follicles that are inductive sites for IgA production.

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5
Q

How do microbes cross the epithelial and enter PPs?

A

M cells.

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6
Q

Which cytokines cause cytotoxicity and delayed type hypersensitivity?

A

IFN-y

TNF

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7
Q

Which cytokines activate neutrophils?

A

IL-17

TNF

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8
Q

What are AMPs and where are they produced?

A

Antimicrobial peptides.

Epithelial cells

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9
Q

What eliminates commensal bacteria? How? (2)

A

Macrophages by production of IL-10 OR DCs producing IL-6/TGF-beta

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10
Q

What cells differentiate once commensal Ags are presented to DCs?

A

Tregs

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11
Q

What cells can upregulate AMPs?

A

Th17

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12
Q

Mucosal firewall

A

Combo of mucus layer, AMPs, IgA, and Dcs, Treg, Th17 that limit passage of commensals to the GALT.

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13
Q

Microbiota in the GI protects against enteropathogenic infection. What can compromise the microbiotic barrier?

A

Malnutrition

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14
Q

3 SCFAs

A

Acetate
Propionate
Butyrate

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15
Q

SCFAs can result in accumulation of:

A

Tregs

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16
Q

PSA derived from B. fragilis acts on Tregs through:

A

TLR2 to promote Treg function by increasing expression of IL-10 and TGF-b

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17
Q

Oral tolerance

A

Suppression of immune responses to Ags that have been administered orally.

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18
Q

Central vs peripheral tolerance

A

CT: immature lymphocytes specific for self Ag are destroyed, changed, or made into Tregs.
PT: Mature self-reactive cells are anergic, deleted, suppressed.

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19
Q

What 3 molecules are of clinical importance in oral tolerance? What do they do overall?

A

TGF-beta
Retinoic acid
IDO
Induce Treg differentiation.

20
Q

4 Steps in the response to Ags in oral tolerance

A
  1. Mo directly take up Ags.
  2. Mo transfer the Ag to DCs.
  3. DCs move from lamina propria to mesenteric LN.
  4. DCs stimulate naive CD4+ T cells differentiate into FOXP3 Tregs.
21
Q

IgE mediated food reactions constitute what type of hypersensitivity?
Non-IgE (IgA or IgG)?

A

Type I

Type III or IV

22
Q

What cell type mediates Non IgE food reactions? When does it occur?

A

T cells

4-28 hrs after eating

23
Q

Tryptase’s role in anaphylaxis

A

Released from activated mast cells that act on C3 and C5 to locally generate C3a and C5a that further activate MCs and exacerbate the sx.

24
Q

What 3 things can suppress inflammation?

A

Vitamin D, A folate

25
Q

What is the effect of a high fat diet on inflammation?

A

It promotes inflammation

26
Q

What cells are suppressed by microbiota?

A

Basophils, MCs

27
Q

Role of iTregs in allergic sensitization

A

Suppresses Th2 cells that generate IgE and allergic effector cells.

28
Q

What’s the most common food allergy?

A

Milk

29
Q

How do peanuts contribute to shock?

A

By causing the production of C3a

30
Q

What does C3a do in anaphylaxis?

A

It stimulates Mo, basophils, and MCs to produce PAF and histamine, which increase vascular permeability and SM contractility.

31
Q

How are allergies tested?

A

Skin tests. If it is negative, then it could be followed by an intradermal test.

32
Q

What enables Ags to trigger distal reactions (urticuria, bronchospasm)?

A

Histamine, PAF

33
Q

GI manifestations of food allergies are dependent on:

A

Th2 derived cytokines

IL-4, IL-13, IL-9

34
Q

What mediates the local acute GI response to allergen?

A

PAF and serotonin

35
Q

Major triggers of type IV hypersensitivity

A

Autoimmunity, environmental Ags, microbial Ags.

36
Q

Type III hypersensitivities are focused around:

A

Complement activation

37
Q

Why are allergies to cow’s milk fairly mild?

A

There is no known IgE specific for cow’s milk protein in human blood.
This would cause the prick test to be negative.

38
Q

What type of hypersensitivity is an allergy to cow’s milk?

A

Type IV (delayed type)

39
Q

Peanut allergies have both:

A

IgE and non IgE mediated mechanisms

40
Q

4 major steps of a nut allergy (food-induced anaphylaxis)

A
  1. MCs activated by IgE and cross-link.
  2. Histamine and PAF are released by MCs and cause sx.
  3. IgG can induce Mo and neutrophils, which also produce PAF.
  4. PAF and histamine increase vascular permeability and SM contractility.
41
Q

B cells and Ag can activate 2 pathways: IgG and IgE.

Which is more severe and what are the 2 subpathways pf IgG?

A

IgE > IgG
IgG can activate complement –> C3a/C5a OR
Mo and activate PAF.

42
Q

Silent CD pt’s test positive in what?

A

Anti-TG2 antibodies

43
Q

What 2 molecules predispose a pt to CD?

A

HLA-DQ2 and DQ8

44
Q

What AAs does gluten have a lot of?

What is the problem with one of them?

A

Proline and glutamine.

There is no enteropeptidase for proline and is poorly broken down.

45
Q

CD pts express which kind of HLA?

A

HLADQ2.5

46
Q

What type of hypersensitivity occurs in CD?

A

Type III

47
Q

Assaying what is most common in clinical practice?

A

TG2-specific IgA

GI Exam #1 (10 decks)

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