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GIGU Midterm > Gut Immunology > Flashcards

Gut Immunology Flashcards

1
Q

what does the gut-associated lymphoid tissue (GALT) consist of?

A

multi-follicular Peyer’s patches and isolated lymphoid follicles (ILF)

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2
Q

what is critical for the GALT and ILT development that in turn regulates the microbiota?

A

cross-talk between the host immune system and the microbiota

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3
Q

what are isolated lymphoid follicles (ILFs)?

A

they are single B-cell follicles that act as an inductive site for IgA production

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4
Q

what is the primary route by which the body is exposed to Ags (microbial and diet)?

A

the GALT

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5
Q

how do the Peyer’s patches and ILFs receive Ags since they lack afferent lymphatic vessels?

A

they receive Ags directly from the epithelial surfave and via Ag-transporting DCs

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6
Q

what is another way that microbes can cross the epithelium and enter the peyer’s patches?

A

through M cells, from which they are endocytosed by DCs in the subepithelial dome

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7
Q

Ag-loaded dendritic cells in the peyer’s patches interact with what to do what?

A

they interact with local lymphocytes to induce differentiation of T cells and T-dependent B cell maturation in the germinal center–> leads to the induction of the development of IgA producing plasma cells

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8
Q

what do goblet cells produce and how is their product organized?

A

they produce mucin, which is organized into a dense inner proteoglycan gel (inner mucous layer)

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9
Q

what cells continually sense the microbiota (MAMPs)?

A

enterocytes in the small intestine, colonocytes in the large intestine and specialized Paneth cells

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10
Q

what do the enterocytes, colonocytes, and Paneth cells induce the production of?

A

antimicrobial peptides (AMPs)

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11
Q

how does the secretory IgA maintain a peaceful bacteria-host interaction?

A

IgA does not activate complement, IgA does not activate phagocytes, and IgA is resistant to proteolysis

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12
Q

what is the major class of AMPs in the GI which represent innate immunity?

A

defensins

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13
Q

why is the inner mucous layer largely impervious to bacterial colonization or penetration?

A

due to its high density and high concentration of bactericidal defensins

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14
Q

describe the structure of defensins?

A

they have clusters of positively charged amino acid side chains and hydrophobic amino acid side chains

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15
Q

what do defensins cause in microbial membranes due to their structure?

A

membrane “wormholes” or pores

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16
Q

what are defensins produced by?

A

epithelial cells

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17
Q

what happens when commensal and pathogenic bacteria penetrate the enterocyte epithelial layer?

A

they are rapidly killed by macrophages in the lamina propria

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18
Q

what is lying over the peyer’s patches? and what happens if bacteria penetrate this?

A

a specialized follicle-epithelium, containing M cells. these bacteria are also rapidly killed by macrophages, but some bacteria can be picked up by DCs

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19
Q

once the DCs pick up antigen, where do they travel?

A

to the draining mesenteric lymph nodes

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20
Q

what do DCs that engulf bacteria induce?

A

IgA producing plasma cells

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21
Q

Although the DCs loaded with commensal bacteria can traffic to the mesenteric LNs, what do the LNs function as?

A

as a barrier, the loaded DCs cannot penetrate further to reach the systemic circulation

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22
Q

following activation, Ag-activated B and T cells leave the mesenteric LNs through the efferent lymph, enter the bloodstream at the thoracic duct and then do what?

A

home back to the intestinal mucosa

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23
Q

in the mesenteric lymph node, the dendritic cell interacts with a naive and does what?

A

stimulates their proliferation

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24
Q

where is the T cell differentiation taking place?

A

in the environment where stromal cells produce a significant amount of TGF-beta

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25
Q

what does the limited expression of pro-inflammatory cytokines by APCs and an excess of TGF-beta result in?

A

differentiation of naive T cells into Tregs

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26
Q

what do T regs suppress?

A

Th1 cells, Th2 cells, and Th17 cells

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27
Q

what has a major effect on gut microflora?

A

changes in diet, environmental factors, and host genetics

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28
Q

what happens to undigested dietary carbohydrates in the gut?

A

they are fermented by gut commensal bacteria to produce SCFAs

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29
Q

what are some examples of SCFAs produced by commensal gut bacteria?

A

acetate, propionate, and butyrate

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30
Q

what is the function of acetate?

A

it stimulates the accumulation of IL-10-producing colonic Tregs

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31
Q

why are SCFAs important?

A

they help to support an effective IgA-mediated response to the gut pathogens and they stimulate the production of mucus

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32
Q

some T cells with high affinity for self antigens will express what?

A

the Foxp3 transcription factor and they will become natural t regulatory cells

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33
Q

since the intestine Ags are not available in the thymus, what can be said about central tolerance?

A

it does not prevent responses against antigens in the lamina propria; therefore additional layers of peripheral tolerance are needed

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34
Q

what group of immune cells have been shown to play a crucial role in induction of oral tolerance?

A

macrophages, dendritic cells, and T regulatory cells

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35
Q

in the mesenteric lymph node, what do DCs stimulate?

A

the naive CD4+ T cells to differentiate into induced CD4+ CD25+ Foxp3+ T regulatory cells

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36
Q

how do DCs stimulate the development of T reg cells?

A

via the release of retinoic acid, TGF-beta, and IDO

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37
Q

what is the role of retinoic acid (RA)

A

it directly induces Treg cell differentiation

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38
Q

what is the role of TGF-beta?

A

it mediates Foxp3 up-regulation in Treg differentiation

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39
Q

what is the role of IDO?

A

it has important immunosuppressive functions, which cause anergy of effector T cells and it induces the proliferation of T reg cells

40
Q

what are the categories of non-immune mediated food adverse reactions?

A

pharmacological, enzymatic, psychosomatic, and irritant

41
Q

what are the categories for immune-mediated food adverse reactions?

A

IgE-mediated (type I) and non-IgE-mediated (type III/IV)

42
Q

what is the most common form of immune-mediated adverse reactions to foods?

A

type I hypersensitivity

43
Q

how is type I hypersensitivity always characterized?

A

by the development of IgE against food allergens

44
Q

how can a patient with an IgE-associated food allergy be identified?

A

based on the detection of food allergen by measuring in vivo IgE-mediated skin reaction to allergen

45
Q

what do type III and type IV hypersensitivities involve?

A

the activation of macrophages by allergen-Ab complexes

46
Q

what might abrogate oral tolerance leading to food allergy?

A

genetic and environmental factors

47
Q

what is sensitization?

A

when the allergen induces IgE production in genetically predisposed individuals

48
Q

what does repeated allergen contact activate?

A

the allergen-specific T cells and induces the IgE dependent secondary immune response

49
Q

after allergen ingestion and degradation, what happens to the allergen fragments?

A

they are internalized from the GI and distributed throughout the body

50
Q

Ag disseminated systemically can trigger distal reactions (urticaria and bronchospasm) through mechanisms dependent on what?

A

histamine and platelet activating factor (PAF)

51
Q

the GI manifestations of food allergy are dependent on what?

A

the Th2- derived cytokines including IL-4, IL-13, and IL-9 (these cause increase in mast cells)

52
Q

what mediates the local acute GI response (diarrhea) to allergen exposure?

A

PAF and serotonin

53
Q

treg cell derived what and what supress what immunity?

A

treg cell derived IL-10 and TGF-beta suppress Th2 immunity and inhibit mast cell reactivity

54
Q

in a person with a food allergy, what happens to their Th2 levels?

A

they are increased

55
Q

what effect do vitamin d and vitamin a have on inflammatory responses?

A

they suppress inflammatory responses

56
Q

what effect does a high fat diet have on inflammatory responses?

A

it promotes inflammation

57
Q

how does the gut microbiota or its constituents suppress allergic immune responses?

A

through the induction of Treg cells and/or direct supression of basophils and mast cells

58
Q

what are central to generating IgE and allergic effector cells?

A

Th2 cells

59
Q

what is the primary tool for assessing immediate hypersensitivity reactions?

A

the patient’s history

60
Q

what type of allergy is wheat allergy?

A

type I hypersensitivity

61
Q

what are the most important allergens involved in wheat allergy?

A

alpha-amylase inhibitors, wheat germ agglutinin, and peroxidase

62
Q

what is the correlation of IgE to wheat with age?

A

the prevalence of IgE to wheat progressively increases with age

63
Q

what is a common symptom of wheat allergy?

A

food-dependent exercise-induced anaphylaxis (FDEIA)

64
Q

what is FDEIA?

A

urticaria or angioedema with upper respiratory obstruction and hypotension precipitated by exercise after ingestion of certain foods in susceptible persons

65
Q

what drugs could cause FDEIA?

A

aspirin and NSAIDs

66
Q

what are some common foods that have caused FDEIA?

A

seafood, celery, wheat, and cheese

67
Q

what is the mechanism behind FDEIA?

A

exercise/aspirin enhance the absorption of undigested immuno-reactive allergens into the circulation; related to permeability

68
Q

non-IgE mediated reactions are delayed and take how long to develop?

A

up to 48 hours

69
Q

what is an example of a non-IgE mediated food allergy?

A

Cow’s milk allergy (CMA)

70
Q

what is the dietary management of a non-IgE CMA?

A

involves removal of all dairy products from diet

71
Q

what is an example of a mixed IgE-mediated food allergy?

A

peanut allergy

72
Q

what is non-IgE mediated allergic reaction to peanuts?

A

it is peanut-induced anaphylaxis mediated in part by IgG-induced activation of macrophages

73
Q

What contributes to a nut-induced allergy and anaphylaxis?

A

IgE-mediated (mast cells) and non-IgE-mediated (IgG induced activation of macrophages)

74
Q

how do peanuts and other nuts in general contribute to shock?

A

by causing production of C3a (complement activation)

75
Q

what does C3a stimulate?

A

macrophages, basophils, and mast cells to release PAF and histamine in a C3aR-dependent manner

76
Q

what are the effects of histamine and PAF?

A

they increase vascular permeability and smooth muscle contractility

77
Q

what are the main genetic predisposing factor for celiac’s diease?

A

the HLA-DQ2 and DQ8 molecules

78
Q

what antibodies are specifically associated with CD?

A

serum autoantibodies against the ubiquitous enzyme tissue transglutaminase 2 (TG2)

79
Q

what is CD strongly linked to?

A

autoimmunity

80
Q

what type of protein is gluten?

A

proline-rich protein that is poorly digested in the small intestinal tract due to a lack of prolyl endopeptidases

81
Q

what is gluten rich in?

A

glutamine residues

82
Q

what does it mean when it is said “deamination of gluten”?

A

some of the glutamines in the peptides can be deaminated by tissue enzyme TG2

83
Q

what happens when gluten is deaminated?

A

the formation of negatively charged glutamic acid residues

84
Q

what serves as the anchor for residues of the peptide that is loaded into HLADQ2.5?

A

the negatively charged glutamine residues

85
Q

in CD, how does tissue damage occur?

A

in a type IV hypersensitivity manner

86
Q

what triggers the cell-mediated immune mechanism in CD patients?

A

gluten-specific T cells that are generated

87
Q

In CD patients, gluten causes a T-cell mediated inflammatory response that generates what?

A

an inflammatory environment and it produces IgA antibodies against gluten (anti-TG2 Abs)

88
Q

what is the result of inflammatory response when T cells are activated and release IFN and TNF?

A

matrix degradation and mucosal remodeling

89
Q

activated gluten-specific CD4 T cells secrete mainly what?

A

Th1 cytokines (IFN)

90
Q

what do Th1 cytokines (IFN) induce?

A

the release of MMPs by myofibroblasts

91
Q

what is the effect of MMPs?

A

mucosal remodeling and villus atrophy

92
Q

what are produced that drive the production of auto-Abs to gluten and TG2?

A

Th2 cytokines

93
Q

other cytokines seem to play a role in polarizing and maintaining the Th1 response. What are they?

A

IL-18, IFN-gamma, or IL-21

94
Q

what is the role of IL-15?

A

it links the adaptive immune system to innate immune responses serving as a growth factor for T cells causing their proliferation

95
Q

what is recommended to be the initial testing for CD?

A

the measurement of IgA antibody to human tissue transglutaminase (tTG)

96
Q

about 95% of patients with CD have which one of the celiac disease associated HLA alleles?

A

DQ2

GIGU Midterm (19 decks)

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