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GIGU Exam 1 > Lecture 17: Gut Immunology > Flashcards

Lecture 17: Gut Immunology Flashcards

1
Q

What is GALT?

A

Gut-associated lymphoid tissue

Part of MALT, which works in the immune system to protect the body from invasion in the gut. It consist of Peyer’s Patches and Isolated lymphoid Tissue (ILT)

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2
Q

What are ILFs

A

Mature crytopatches that develop in the SI & LI after birth. They are single B-cell follicles that act as inductive site for IgA production

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3
Q

How does GALT receive antigens?

A

Directly from epithelial surface and dendritic cells

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4
Q

Microbes crossing the epithelium enter Peyer’s Patches through what cells?

A

M cells - microbes are endocytosed by dendritic cells from here

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5
Q

What happens when dendritic cells bind to an Ag in Peyer’s patches

A

Dendritic cells interact with T-cells and T-cell-dependent B cells, promoting the maturation of B cells into IgA-prooducing plasma cells

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6
Q

What do B cells mature into and what do they release in the gut?

A

IgA producing plasma cells

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7
Q

What promotes the development of mature ILFs (isolated lymphoid follicles)?

A
  1. MAMPs recognized by PRRs (pattern-recognition receptors)
  2. Stimulate recruitment of B and T cells
  3. Cryptopatches develop into mature ILFs
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8
Q

What are Paneth Cells?

A

Cells found in the small intestine that have antimicrobial properties similar to neutrophils

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9
Q

What are defensins and what produces them?

A

Antimicrobial peptides that contribute to mucosal host defense of the GI system which plays an important role in innate immune system. They are produced by enterocytes, colonocytes but largely by Paneth cells

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10
Q

What are the major class of anti-microbial peptides (AMPs) in the GI that represent INNATE IMMUNITY

A

Defensins

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11
Q

List the intestinal epithelial cells.

A
  • Goblet Cells: Produce dense mucin
  • Enterocytes: main cells in SI
  • Colonocytes: main cells in the LI
  • Paneth Cells: Found in crypts of SI that sense microbiota to induce production of antimicrobial peptidens (defensins)
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12
Q

What is the role of secretory IgA (sIgA) and how does it do it?

A

Maintains a peaceful bacteria-host interaction:

  • does not activate complement system
  • does not activate phagocytosis
  • resistant to proteolysis
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13
Q

How do defensins work?

A

Has both hydrophobic and hydrophilic parts that allows it to disrupt microbial membranes and form pores

INNATE IMMUNITY

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14
Q

Where do most of the commensal bacteria reside?

A

Outside the layer of mucus covering intestinal epithelial cells

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15
Q

What kills commensal and pathogenic bacteria that penetrate epithelial layer?

A

Macrophages in lamina propria

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16
Q

What happens if dendritic cells pick up antigens?

A

Enables DCs to activate B and T cells or they migrate to the draining mesenteric lymph nodes

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17
Q

Dendritic cells that engulf bacteria induce what

A

IgA-producing plasma cells

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18
Q

Can Ag bound dendritic cells eventually reach systemic circulation?

A

No, mesenteric lymph nodes function as a barrier. Loaded DCs cannot penetrate farther to reach the systemic circulation

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19
Q

What happens to B and T cells after activation?

A

Unlike DCs, they can leave mesenteric lymph nodes through efferent lymph, enter the blood stream at the thoracic duct and home back to the intestinal mucosa

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20
Q

What is the significance of short chain fatty acids

A

Important source of energy for colonocytes

  • from colonic microbial fermentation of dietary fibers
  • promote differentiation of Tregs
  • stimulate production of mucus
  • support effective IgA mediated response to pathogens
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21
Q

What does acetate stimulate?

A

Accumulation of IL-10 producing Tregs

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22
Q

What does butyrate stimulate?

A

Directly acts on Tregs or modulates DC function to enhance Treg-inducing ability

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23
Q

What is the function of capsular polysaccharide A (PSA)

A

Promote Treg function by enhancing expression of effector molecules including IL-10 and TGF-beta

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24
Q

What is immune tolerance?

A

Sustained immune unresponsiveness to self-antigens, beneficial antigens, and commensal bacteria.

Not attacking self or good bacteria

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25
Q

What is oral tolerance?

A

Suppression of immune responses to antigens that have previously been administered orally

26
Q

If immune or oral tolerance is disturbed, what can that lead to?

A

Food allergies and Celiac Disease

27
Q

What is central tolerance?

A

Immature lymphocytes that select self-antigens in central lymphoid organs are deleted or develop into Treg cells

28
Q

What is peripheral tolerance?

A

Self-reactive lymphocytes in peripheral tissues are inactivated, deleted, or suppressed by Treg cells

29
Q

Why is peripheral tolerance to Ags in the intestine important

A

Intestine antigens are not available in thymus so central tolerance does not prevent responses against Ags in the lamina propra

30
Q

Describe the mechanisms of oral tolerance.

A
  1. Macrophages take antigens from intestinal lumen across epithelial barrier or DCs directly take up Ags.
  2. Macrophages transfer antigens to dendritic cells in lamina propria
  3. Dendritic cells with antigens go to mesenteric lymph nodes
  4. DCs stimulate naive CD4+ T cells into Treg cells via the release of retinoic acid (RA), TGF-beta and IDO
31
Q

What are Tregs?

A

Suppress immune response, thereby maintaining homeostasis and self-tolerance

32
Q

What are examples of non-immune mediated adverse reactions?

A
  1. Absence of an enzyme (e.g. lactose intolerance)
  2. Irritable Bowel Syndrome
  3. Food poisoning
  4. Recurring stress or psychological factors
33
Q

What are examples of immune mediated adverse reactions?

A
  1. Food allergies
  2. Celiac Disease: triggered by gluten
  3. Sensitivity to food additives
34
Q

What type of hypersensitivity is most common with food allergies?

A

Type I Hypersensitivity -characterized by IgE antibodies against food allergens

Type 3 and 4 is also possible

35
Q

Describe the primary allergen ecounter

A
  1. Allergen is ingested
  2. Adaptive immune response by B cells that mature into plasma cells to make IgE
  3. IgE enters circulation and is rapidly bound by CD23 on mast cells in tissues
36
Q

Describe a secondary response to a food allergen.

A

After recurrent contact with an allergen, IgE-dependent secondary immune response activated. The allergen is degraded and fragments are distributed throughout the body –> response in skin, respiratory tract, and circulatory tract

37
Q

What are some mediators of an early allergic reaction?

A

Histamine

Tryptase

Bradykinin

38
Q

What are some mediators of a late allergic reaction?

A

Prostaglandins

TNF-alpha

Leukotrienes

Various interleukins

39
Q

How do disseminated antigens trigger distal reactions?

A

Mechanisms dependent on histamine and platelet activating factor (PAF) -urticaria (hives) -bronchospasm

40
Q

What cytokines are GI manifestations of food allergies dependent on?

A

Th2 derived cytokines: IL-4, IL-13, IL-9

41
Q

What do response to local GI allergen exposure do platelet activating factor (PAF) and serotonin mediate?

A

Diarrhea

42
Q

What is the central role of Treg cells in controlling food allergies?

A

1) Secrete IL-10 and TGF-β to suppress Th2
2) Inhibit mast cell reactivity
3) Reduce IgE synthesis
4) Increase IgG and IgA synthesis

43
Q

What vitamins suppress inflammatory responses?

A

Vitamin D

Vitamin A

Folate

44
Q

What promotes inflammation

A

high fat diet

45
Q

What are involved in an allergey

A

IgE

basophils

mast cells

46
Q

What can suppress allergic immune responses

A
  1. Gut microbiota
  2. Direct suppression of basophils and mast cells
  3. Tregs supressing Th2 cells (generate IgE and allergic effectors)
47
Q

What are some ways to diagnose an IgE mediated allergy?

A

Testing Type 1 Hypersensitivities:

  1. Skin Prick Test
  2. Serum-specific IgE test
  3. Atopy Patch
  4. Basophil activation test
48
Q

How does anaphylaxis occur in those with peanut allergies?

A

IgE mediated: Mast cells are activated by IgE cross-linking FceRI

Non-IgE mediated: IgG1 induced activation of Mf Mediators (histamine and PAF) released by mast cells

49
Q

Describe the non IgE mediated allergic reactions to peanuts.

A

ARE DELAYES AND TAKE UP TO 48 HOURS TO DEVELOP - TYPE IV SENSITIVITY

  1. Peanuts stimulate production of C3a
  2. C3a stimulates production of macrophages, basophils, and mast cells
  3. PAF and histamine released
  4. Increase in vascular permeability and smooth muscle contractility.
50
Q

What allergens mosty cause a wheat allergy?

A

α-amylase inhibitors

agglutinin

peroxidase

51
Q

Majority of infants with an allergy to cow’s milk have what type of allergy?

A

non-IgE-mediated allergy -can take up to 48 hours to develop

52
Q

What is celiac disease?

A

Systemic immune disorder caused by permanent sensitivity to gluten

53
Q

What amino acids is gluten rich in

A

proline and glutamate

54
Q

Which HLA molecules are the main predisposing factor in developing celiac disease?

A

HLA-DQ2 and HLA-DQ8

55
Q

In Celiac Disease, what autoantibodies are found?

A

anti-Tissue Transglutaminase 2 antibodies (TG2)

56
Q

What is the purpose of Transglutaminase 2 (TG2)?

A

Deamination of glutamine found in gluten

57
Q

What type of hypersensitivity is Celiac Disease?

A

Type IV Hypersensitivity

58
Q

Describe the pathogenesis of Celiac Disease

A
  1. Activated gluten specific CD4 T cells secret TH1 IFN-gamma that release MMPS resulting in mucosal remodeling and atrophy
  2. Additionally, TH2 cytokines are produced driving the production of auto-Abs to gluten and TG2
59
Q

What links the adaptive immune system to the immune response of celiac dissease and how does it do it?

A

IL-15 by serving as a growth factor for T cells causing their proliferation

60
Q

What is the best way to test for Celiac Disease?

A
  • tTG-IgA test
  • Intestinal biopsy to confirm the diagnosis
  • Presence of DQ2 or DQ8 allele

GIGU Exam 1 (25 decks)

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