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GIGU > Gut Immuno > Flashcards

Gut Immuno Flashcards

1
Q

What is the function of the immune system in the intestine?

A

Must discriminate between harmful pathogens and tolerance to harmless microflora and diet antigens

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2
Q

What is associated with a growing number of intestinal diseases?

A

Disruption of gut microbiota

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3
Q

What early-life exposures contrinbute to colonization of infect intestines?

A 
Maternal Microbes
Infant Diet
Abx
Probiotics (enrichment)
Environmental Microbes
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4
Q

What are examples of gut microbiota symbiosis?

A

Immune tolerance
Intestinal homeostasis
Healthy metabolism

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5
Q

What are examples of gut microbiota dysbiosis?

A
  • Immune disease (asthma, MS)
  • Intestinal disease (IBS)
  • Metabolic disease (DM, obesity)
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6
Q

What is the largest immune organ in the body?

A

Gut-associated lymphoid tissue (GALT)

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7
Q

What do GALT consist of?

A

Peye’s patches and isolated lympoid tissue (ILT)

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8
Q

What is critical for GALT and ILT development–> regulate microbiota?

A

Cross-talk between host immune system and microbiota

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9
Q

When/where do ILT develop?

A

after birth in small and large intestines

—>dynamic response of gut immune system to microbiota

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10
Q

How is the body expose to microbial and diet antigens in the gut?

A

GALT

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11
Q

How do peyer’s patches and ILT receive antigens directly from the epithelial surface?

A

antigen-transporting dendritic cells

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12
Q

Why do peyer’s patches and ILT receive antigens directly from the epithelial surface?

A

They lack afferent lymphatic vessels (incoming)

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13
Q

How are B cells and T cells recruited in the gut?

A

Microbe-associated molecular patterns (MAMPs) on intestinal epithelial and DCs are recognized and stimulate recruitment

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14
Q

How do ILF mature?

A

MAMPs recognized–>recruit B and T cells–> cryptopatches develop into mature ILFs

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15
Q

What are ILFs?

A

Single B-cell follicles that act as inductive site for IgA production

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16
Q

What occurs when MAMPs are sensed?

A

Stimulates proliferation of intestinal epithelial cells in crypts–> increase depth, increase density of Paneth cells in SI

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17
Q

How are defensins primed for release?

A

sensing of MAMPs

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18
Q

What contribute to antimicrobial action and mucosal defense in GI?

A

Defensins (antimicrobial peptides)

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19
Q

What occurs when DC in peyer’s patches interact with local lymphocytes?

A

induce diff of T cells and T-dependent B cell amturation in germinal cells–> IgA-producing plasma cells so IgA can transpor into intestinal lumen

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20
Q

What cells produce mucin that organizes into dense proteoglycal gel on intestinal epithelial cells?

A

Goblet cells

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21
Q

What continually sense microbiota and induce production of antimicrobial peptides (AMPs)?

A

Eneterocytes, colonocytes, Paneth cells in bases of SI crypts

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22
Q

WHat are major classes of AMPs in GI?

A

Defensins

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23
Q

How does secretory IgA maintain peaceful bacteria-host interaction?

A

IgA:

  • does not activate complement
  • does not activate phagocytes
  • resistant to proteolysis by peptidases in GI

–> why major fxn of GI is exclusion (if + completement, damage intestines)

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24
Q

How is the inner mucous layer impervious to bacterial colonization?

A

High density and concentration of bactericidal defensins

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25
Q

What provides protection against 98% of pathogens encountered in body?

A

innate immune system

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26
Q

How do defensins produce pores in pathogen membranes?

A

have charged and hydrophobic aa chains that interact with microbial membranes–> pores–>kill pathogen

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27
Q

Where do the large number of commensal bacteria reside in the gut?

A

outside the layer of mucus that covers intestinal epithelial cells

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28
Q

What happens to commensal and pathogenic bacteria that penetrate the intestinal epithelial layer?

A

Rapidly killed by macrophages in lamina propria

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29
Q

How can activated B and T cells (via DC) return to intestinal mucosa?

A

Activation by DC with bacteria that invaded Peyer’s patches–> leave mesenteric LN via efferent lymph–> bloodstream at thoracic duct–> back to intestinal mucosa

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30
Q

Describe how DC pick up bacteria in the gut

A

Bacteria that penetrate M cells overlying Peyer’s patches are RAPIDLY KILLED by macrophages, but can be picked up by DC

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31
Q

What do DC do with bacteria that penetrated Peyer’s patches?

A

Migrate to draining mesenteric LN–> activate T and B cells, + IgA-producing plasma cells

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32
Q

Why can’t DC reach the systemic circulation from the gut?

A

LN function as a barrier so DC with either pathogenic or commensal bacteria can’t penetrate to reach bloodstream

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33
Q

What make up 10% of T cells in GALT?

A

Treg cells (anti-inflammatory)

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34
Q

What is the function of Treg cells in the GI?

A

limited pro-inflamm cytokines and excess TGF-B (from lamina propria)—> diff of T cells into Treg cells–> SUPPRESS Th1, 2 and 17 responses

*****ANTI-INFLAMMATORY

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35
Q

How can dysbiosis occur?

A

Changes in diet and environmental factors

–> change composition of microflora and connections of epithelial cells

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36
Q

What are examples of short-chain fatty acids?

A

butyric acid, propionic acid, acetic acid

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37
Q

What is produced by colonic microbial fermentation of undigested (or partially) dietary fibers?

A

short-chain fatty acids (SCFAs)

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38
Q

Why is an infant born of C-section more likely to have GI disorders within first few years of life?

A

Wasn’t exposed to mother’s microflora—> infant has underdeveloped gut microflora

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39
Q

What recognize MAMPs?

A

Pattern recognition receptors (PRRs)

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40
Q

How do IgAs work in gut?

A

Form single layer on top of epithelial cells, multiple bind to bacteria

–> if bacteria try to penetrate, create respiratory burst–> release of toxins that destroy pathogens

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41
Q

How to antigens from diet interact with cells in the gut?

A

Go to subepithelial dome of M cells and Peyer’s patches where they are picked up by DC–> migrate to draining mesenteric LB–> interact with T and B cells

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42
Q

What is undernutrition associated with?

A

defects in innate and adaptive immunity

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43
Q

Recurrent enteric infections predispose you to?

A

nutrient deficiencies and impaired intestinal mucosal barrier fxn—> increase susceptibility to inf even more

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44
Q

Why is malnutrition so harmful to the gut?

A

Microbiota acts as barrier to pathogen infection–> disrupted by malnutrition

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45
Q

Generally, what is the function of SCFA?

A

promote Treg diff and sIgA production

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46
Q

Fxn of acetate

A

+ accumulation of IL-10 and colonic Tregs

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47
Q

Fx of butyrate

A

acts directly on Tregs or via modulation of DC–> enhance Treg-inducing ability of DC

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48
Q

What acts on Tregs via TLR2 (promotes fxn, enhances IL-10 and TGF-B)

A

Capsular polysaccharide A (PSA)

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49
Q

What fxn do SCFAs have on mucus and IgA

A
  • support effective IgA-mediated response to gut pathogens

- stimulates production of mucus (maintains barrier)

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50
Q

Define immune tolerance

A

sustained immune UNRESPONSIVENESS to self-AG, beneficial AG and commensal bacteria

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51
Q

Define oral tolerance

A

suppression of immune responses to Ag that have been administered previously by oral route

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52
Q

What occurs due to failure of induced tolerance to food protein (oral tolerance)?

A

food allergy, celiac disease

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53
Q

What is the most prevalent food-induced pathology?

A

Celiac disease

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54
Q

Define central tolerance

A

immature lymphocytes specific for self AG–> encounter Ag in central lymp organs—–> are deleted, change B cell specificity, develop into Treg cells

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55
Q

Define peripheral tolerance

A

Mature self-reactive lymphocytes in periphery–> inactivated (anergy), deleted, suppressed by Treg cells

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56
Q

Generally, why is peripheral tolerance required over central in the gut?

A

Intestine Ag not available to cells in thymus (can’t be changed by central tolerance)

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57
Q

What happens to the large number of developing lymphocytes that react against self-Ags and Ags from food/ commensal bacteria?

A

Eliminated in thymus via CENTRAL tolerance

OR express Foxp3 if high affinity for self-Ags–> become natural Treg cells (nTregs)

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58
Q

What normally prevents deleterious immune responses against self-Ag in the body?

A

Central tolerance (developing cells eliminated or neutralized in thymus that react to self-Ag)

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59
Q

Why can’t central tolerance work in the gut?

A

Intestinal Ags can’t go to thymus, so it can’t prevent responses against Ag in the lamina propria

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60
Q

Depletion of what cells inhibits oral tolerance?

A

CD25+ Treg cell

61
Q

What cells can activate oral tolerance?

A

CD4+ CD25+ Treg cells (produced in thymus)

62
Q

What mechanism showed + of suppressor fxn that predated Foxp3 and nTreg cells?

A

induction of T cells with active suppressor fxn in oral tolerance

63
Q

What cells critical for oral tolerance?

A

Macrophages, DC, Treg cells

64
Q

Describe the overall mechanism of oral tolerance

A

Macrophages directly take up Ag from intestinal lumen–> transfer Ag to DC in lamina propria–> go to mesenteric LN–> stimulate native CD4+ T cells~~~~ converted to CD4+ CD25+ Foxp3+ Treg cells

65
Q

How are CD4+ T cells induced to CD4+ CD25+ Foxp3+ Treg cells?

A

release of retinoic acid, TGF-B and IDO via DC s

–> acid induces Treg cell diff

–> TGF-B mediates Foxp3 upreg

–> IDO immunosuppressive fxn causes anergy of effector T cells (induces prolif of Treg cells)

66
Q

Fxn of IDO in oral tolerance

A

immunosuppressive fxn causes anergy of effector T cells (induces prolif of Treg cells)

67
Q

Fxn of retinoic acid in oral tolerance

A

induces Treg cell differentiation

68
Q

Fxn of TGF-B in oral tolerance

A

mediates Foxp3 upregulation in Treg differentiation

69
Q

Non-immune mediated food adverse rxn

A

Food intolerance

70
Q

Immune-mediated food adverse rxn

A

food allergy

71
Q

Toxic vs Non-toxic

A

Toxic:
-bacterial superantigens and staph food poisioning

Nontoxic:
-pharm, psychosomatic, enxymatic= non-immune mediated

-IgE mediated (type 1) and Non-IgE mediated (type 3/4)

72
Q

Examples of non-immune mediated adverse rxn

A

Absence of enzyme needed to fully digest food

IBS

Food poisoning

Recurring stress or psych factors

73
Q

Examples of immune-mediated adverse rxn

A

food ALLERGY, celiac disease via specific immune response (exposure to given food)

Sensitivity to food additives

74
Q

What is a chronic digestive condition triggered by the protein gluten?

A

Celiac disease

—> NOT AT RISK for anaphylaxis d/t mostly GI sx

75
Q

What are most common forms of immune-mediated adverse food reactions?

A

Type 1 hypersensitivity

76
Q

What is the mechanism behind food allergy (generally)?

A

Development of IgE against food allergens

77
Q

Describe the general mechanism of type 3/4 hypersensitivities (food allergy)

A

macrophage activation by allergen-antibody complexes in FcyR dependent manner

–> also + of allergen-specific T cells

78
Q

What can lead to food allergies?

A

genetic disposition, environmental factors that inhibit oral tolerance

79
Q

How many people do food allergies affect?

A

5% young children, 3-4% adults

–> increasing prevalence

80
Q

What are sx of food allergies?

A

skin sx, GI and resp sx

81
Q

How does a food allergy turn into anaphylaxis?

A

After ingestion and degradation, allergen fragments are internalized in GI and distributed throughout body

82
Q

Describe the primary allergen encounter

A

Ingested allergen–> adaptive immune response via B cells (Th2) –> mature into plasma cells–> produces IgE to allergen (IL-4-> IgE) –> IgE in circulation–> bound by mast cells in tissues (FcRe/CD23)

83
Q

Describe the secondary allergen exposure

A

Cross-linking of allergen to mast cell causes it to release vasoactive amines, cytokines, lipids—-> vascular SM contraction, endothelial vasodilation, leukocyte chemotaxis and activation

84
Q

Define allergic sensitization

A

IgE-associated food allergies that appear in early childhood

85
Q

What individuals produce IgE production upon allergen contact to GI, resp or skin?

A

Those who are genetically predisposed

86
Q

What causes IgE-dependent secondary immune response in allergy pathway?

A

Repeated allergen contact–> activates allergen-specific T cells that induce IgE response

87
Q

What factors are important for primary sensitization and boosting of secondary immune responses?

A

things that affect integrity of EPITHELIAL BARRIER and extent of ALLERGEN DIGESTION

88
Q

What mast cell-derived mediators cause early allergic reaction?

A
  • Preformed: HISTAMINE, TNFa
  • Bradykinin, PAF
  • Granule associated: tryptase, chymase, peroxidase

***already make in mast cells

89
Q

What mast cell-derived mediators cause late allergic reaction?

A

IL-1, 2, 3, 4, 5, 6
GM-CSF
TNFa

*****must be synthesized

90
Q

What is the function of histamine in allergic rxn?

A

SM contraction, vascular permiability

91
Q

What are the fxns of TNFz and IL-1 in allergic rxn?

A

endothelial cell inflammation

92
Q

What is the fxn of tryptase in allergic rxn?

A

anaphylais, urticaria

93
Q

What is the fxn of prostaglandin E2 in allergic rxn?

A

Pain, vascular permeability

94
Q

What is the fxn of IL-5 in allergic rxn?

A

sputum eosinophils

95
Q

What is the fxn of bradykinin in allergic rxn?

A

Vasodilator, SM contraction

96
Q

What cells are central to both local and systemic food allergy sx?

A

Mast cells

97
Q

Systemic allergen reactions

A

urticaria (hives), bronchospasm

98
Q

What mediates systemic allergen rxns?

A

Histmaine, platelet activating factor

99
Q

What are GI manefistations of food allergies dependent on?

A

Th2-derived cytokines (IL-4, 9, 13)

100
Q

What is necessary for local sx of food allergies?

A

mastocytosis (accumulate in skin/organs)

101
Q

What mediate local acute GI sx (diarrhea) to allergen exposure?

A

platelet activating factor (PAF), serotonin

102
Q

Systemic vs Local mediators via mast cells

A

Systemic: Histamine, PAF

Local: Serotonin, PAF

103
Q

Role of Treg cells in control of food allergy

A

IL-10 and TGF-B suppress Th2 immunity–> inhibit mast cell reactivity–> REDUCE IgE synthesis–> may increase IgG and IgA

104
Q

What compounds suppress inflammatory responses in allergic sensitization?

A

Vitamin D
Vitamin A
Folate

105
Q

What aspect of diet promotes inflammation?

A

High-fat diet

106
Q

What are IgE, basophils and mast cells involved in?

A

Allergy

107
Q

How does gut microbiota suppress allergic immune response?

A
  • Induce Treg cells

- Directly suppress basophils and mast cells

108
Q

What is the fxn of Th2 in allergy?

A

central to generating IgE and allergic effector cells

109
Q

How to diagnose type 1

hypersensitivitiy allergy

A

1: skin prick test (in facility in case of anaphylaxis)
2: Serum-specific IgE test
3: Atopy patch (eczema)
4: Basophil activation test (BAT)-more research setting

110
Q

What indicates a postitive skin prick test?

A

redness and swellin 20-30 min after exposure to allergen

111
Q

What is the primary tool for assessing immediate hypersensitivity reactions?

A

History

d/t blood or skin prick test not conclusive, must combine to dx allergy

112
Q

Are blood tests more or less sensitive vs skin prick test for allergy dx?

A

less sensitive, but neither conclusive

113
Q

What is considered the gold standard for food allergy dx?

A

oral food challenge

114
Q

What is an example of an allergen-specific IgE that is used to dx allergy via blood test?

A

Peanut-specific IgE

115
Q

Describe the pathway of a peanut allergy

A

Allergy–> DC attach to peanut-specific T cells–> T cells converted to Th2 cell–> release IL-4, 5, 13–> B cells activated–> produce peanut-specific IgE–> attach to mast cells–> release histamine (early) and serotonin (late) that affect local and systemic sx

116
Q

Describe Non-IgE-Mediated allergic rxn to peanuts

A

Peanut and other nuts contribute to shock via production of C3a–> + macrophages, basophils, mast cells to release PAF and histamine via C3aR-dependent pathway (not IgE)

117
Q

What is central part of food-induced anaphylaxis

A

mast cells + by IgE cross-linking of FcERI

118
Q

What is central part of peanut-induced anaphylaxis?

A

IgG1-induced activation of Mf

119
Q

Which response to B cells + Allergen is bigger: IgG1, IgE or complement activatoin?

A

IgE

120
Q

What are the 3 possible pathways of nut-induced anaphylaxis?

A

IgG1–> Allergen-Ab complexes activate macrophages via FcyR1–> release PAF

IgE–> allergen to mast cell via FcERI–> release PAF and histamine

Complement activation–> C3a/C5a–> activates mast cells via their complement receptors–> histamine and PAF

121
Q

What are the most important allergens in wheat allergy?

A

Alpha-amyalse inhibitors

Germ agglutinin

Peroxidase

122
Q

What do wheat allergies affect?

A

skin, GI, resp

–> wheat-dependent, exercise-induced anaphylaxis

–> occupational asthma (baker’s asthma)

–> rhinitis

–> contact urticaria

123
Q

Does prevalence of wheat allergy increase or decrease with age?

A

progressively increases with age (0.4% occurrence in US)

124
Q

Describe sensitization to wheat allergy

A

Eye/Nasal/Oral/Skin exposure + genetics + microbiome + environmental factors–> Th2 and IgE

125
Q

Food-Dependent Exercise-Induced Anaphylaxis

A

ingest certain foods (seafood, celery, whea, cheese) before physical activity (within 2 hours) enhances absorption of undigested immunoreactive allergens into circulation

****can also occur with aspirin and NSAIDs

126
Q

How long do non-IgE mediated allergic reactions take to develop?

A

up to 48 hours, still involve immune system

127
Q

Is cow’s milk allergy IgE or non-IgE mediated?

A

can be either, but majority of infants non-IgE

128
Q

Do infants suspected of non-IgE milk allergy need testing for IgE to milk?

A

no

129
Q

What is non-IgE milk allergy wrongly labelled as?

A

symptoms of lactose intolerance

130
Q

Does an infant with suspected IgE milk allergy need testing for IgE to milk?

A

Yes, via skin prick or blood test

131
Q

What is celiac disease?

A

Systemic immune disorder caused by permanent sensitivity to gluten

  • –> GI sx
  • –> higly variable non-GI sx (failure to thrive, delayed puberty, autoimmune, inflamm, neuro and metabolic disorders)
132
Q

What are the main genetic predisposing factors for celiac disease?

A

HLA-DQ2 and DQ8

—> + adaptive immune responses against gluten peptides

133
Q

Serum autoantibodies against what enzyme are specifically associated with celiac disease?

A

tissue transglutaminase 2 (TG2)

—–> deaminases glutamine residues of gluten

134
Q

There is a strong link between celiac disease and

A

autoimmunity

—> 15-20% CD patients have or will develop autoimmune diseases

135
Q

Describe silent CD presentation

A

95% undiagnosed, most relatives of patients with known CD

—> most found to be positive for anti-gTG2 antibodies

136
Q

What is the prevalence of CD?

A

1%, most remain undiagnosed but can present at any age

137
Q

What antigen is proline-rich and poorly digested in SI?

A

gluten (rich in glutamine)

—> 10-50 aa left incompletely digested

138
Q

Tissue damage in CD occurs in a manner similar to what hypersinsitivity?

A

type 4

–> chronic inflammation with continued gluten ingestion

139
Q

Describe antibody response in CD

A

Gluten (anti-TG2 Ab)–> T cell-mediated inflammatory response in proximal small bowel–> damages mucosa–> malabsorption

140
Q

If everyone has gluten peptides, why doesn’t everyone have CD?

A

Only CD patients have HLA-DQ2.5

141
Q

Pathogenesis of CD

A

Gluten peptides–> cross-link and deamidation via TG2–> presented via HLA-DQ2.5 or 8 on APCs–> activate CD4 T cells–> Th1 cytokines (INFy)–> release of MMPs by myofibroblases–> mucosal remodeling and atrophy

142
Q

How do autoantibodies to gluten form?

A

Th2 cytokines drive production of auto-Ab to gluten and TG2

143
Q

What cytokines mediate Th1 response in CD?

A

IL-18, IFNy, IL-21

144
Q

What links adaptive and innate immune responses in CD and as growth factor for T cells?

A

IL-15

145
Q

Who to test for CD?

A

children that present with failure to thrive, GI sx, non-GI sx

–> IgA Ab to transglutaminase (tTG)```````high sensitivity

146
Q

Why is AGA test no longer recommended for CD dx?

A

inferior accuracy

147
Q

What is helpful to identify unusual case of seronegative CD?

A

intestinal biopsy, recommended to confirm dx of CD

148
Q

When is CD virtually excluded as dx?

A

if lack HLA DQ2 or 8 alleles

GIGU (37 decks)

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