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I&I WC1 > Enterology > Flashcards

Enterology Flashcards

1
Q

What are distinctive features of the mucosal immune system? (7)

A
  1. Intimate interactions between epithelia & lymphoid tissues
  2. Discrete compartments of lymphoid tissue
  3. Specialized antigen-uptake mechanisms
  4. Activated/memory T-cells predominate even in absence of infection
  5. Non-specifically activated natural effector/regulatory T-cells present
  6. Active downregulation of immune responses
  7. Inhibitory macrophages and tolerance-inducing DCs
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2
Q

What are the specialized lymphoid tissues in the small intestine & colon?

A

Small intestine = Peyer’s patches
Colon = colonic patches & isolated lymphoid follicles

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3
Q

Why are lymphoid-like structures directly present in the mucosal surfaces of the intestine?

A

Lymph nodes are relatively far away -> presence of lymphoid structures in the intestines allows for rapid responses

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4
Q

What is the specialized antigen-uptake mechanism of Peyer’s patches?

A

M-cells

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5
Q

What is the function of M-cells?

A

Selective antigen-uptake in the intestine

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6
Q

What kind of T-cells predominates in the intestine? What is the advantage of this?

A

Memory cells -> primed phenotype, allows for rapid responses

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7
Q

Where are memory T-cells in the intestine located?

A

Lamina propria

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8
Q

How is tolerance to food antigens (mainly) maintained in the intestine?

A

Tregs

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9
Q

How are intestinal epithelial cells interconnected?

A

Tight junctions

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10
Q

Which three distinct areas can be distinguished in Peyer’s patches?

A
  1. Dome area containing DCs
  2. T-cell areas
  3. B-cell areas
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11
Q

Where are DCs located in the Peyer’s patches?

A

Dome area

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12
Q

True or false: Peyer’s patches and colonic patches have the same organization

A

False; Peyer’s patches have distinct tissue organization, whereas colonic patches are more loosely organized

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13
Q

Which cell types can be found in the intestinal lamina propria? (4)

A
  1. Memory T-cells
  2. Memory B-cells
  3. High amounts of macrophages and DCs
  4. Relatively low amounts of monocytes
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14
Q

True or false: the composition of immune cells in the lamina propria is the same across the whole digestive tract

A

False; the composition is site-dependent

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15
Q

What are IELs? Where are they mainly found?

A

Intra-epithelial lymphocytes; almost exclusively found in the small intestine, very little in the colon

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16
Q

What is the role of IELs?

A

Have a role in barrier function of the epithelium

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17
Q

How do antigens from the intestines reach lymph nodes?

A

Peyer’s patches and colonic patches contain lymph ducts that drain to mesenteric lymph nodes

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18
Q

What is the function of villi of intestinal epithelium?

A

Surface enlargement

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19
Q

What are the functions of microvilli of the intestinal epithelium? (2)

A
  1. Enlarge surface
  2. Prvent bacterial attachment
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20
Q

What do the villi of the duodenum look like?

A

High villi

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21
Q

What are Brunners glands? Where are they found, and what are their function?

A

Glands in the submucosa of the duodenum -> secrete alkaline solutions to neutralize stomach acid

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22
Q

What can be said about the folds of the jejunum as compaired to the duodenum? What happens to the folds more distally?

A

Higher folds, that lower distally

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23
Q

What happens to the crypts of the ileum, the more distal you get?

A

Crypts deepen towards the ileum

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24
Q

True or false: the ileum has plicae

A

False; the ileum barely has any folds

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25
Q

Where are Peyer’s patches mainly found?

A

Ileum

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26
Q

Why are Peyer’s patches mainly found in the ileum, and not more proximal?

A

Barely any bacteria in the duodenum/jejunum

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27
Q

Why does the colon not contain villi or folds?

A

No need to take up nutrients

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27
Q

Which cell type can be found at the bottom of colonic crypts?

A

Stem cells

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27
Q

Which cell types can be found in the intestinal epithelium? (4)

A
  1. Enterocytes
  2. Goblet cells
  3. Paneth cells
  4. Stem cells
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27
Q

What is the function of enterocytes?

A

Resorption of nutrients

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28
Q

What is the function of goblet cells?

A

Production of mucus

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29
Q

The colon contains [less/more] goblet cells than the small intestine

A

More

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30
Q

Where are goblet cells located in the small intestine?

A

Base of the villi

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31
Q

Where in the intestine can one find Paneth cells under physiological circumstances?

A

Small intestine

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32
Q

What is the function of Paneth cells?

A

Keeping crypts free of bacteria through the release of anti-microbial peptides

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33
Q

True or false: Paneth cells are the only intestinal cells producing AMPs

A

False; other epithelial cells also produce AMPs, but in far lower amounts

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34
Q

What happens when a Paneth cell is unable to clear bacteria?

A

Sensing of bacteria using TLRs & PRRs -> signals for assistance

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35
Q

In which instance can Paneth cells be found in the colon?

A

Paneth cell metaplasia -> occurs in severe colonic disease

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36
Q

How long does regeneration from crypt to villus take?

A

~36 hours

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37
Q

How do intestinal microbiota contribute to host physiology? (4)

A
  1. Bacteria facilitate digestion & absorption of nutrients
  2. Bacteria-derived signals are needed for normal intestinal physiology
  3. Commensal bacteria limit pathogen colonization
  4. Host provides a protected & nutrient-rich environment
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38
Q

Which two systems in the intestine are dependent on the presence of signals from intestinal microbiota?

A
  1. Epithelium
  2. Immune system development
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39
Q

Which constituent parts form the intestinal epithelial barrier, which limits bacterial penetration of host tissue? (5)

A
  1. Microvillar extension -> prevent bacterial attachment
  2. Epithelial tight junctions
  3. Mucinous secretions by goblet cells
  4. Epithelial transcytosis of IgA
  5. Antimicrobial peptides
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40
Q

True or false: epithelial tight junctions in the intestine always remain tightly closed

A

False; they can be opened in a controlled way, but without breaking the barrier

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41
Q

What is the main component of mucus?

A

Polysaccharides

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42
Q

The [small intestine/colon] has a thicker mucus layer

A

Colon has a thicker mucus layer

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43
Q

What does a lack of mucus-production lead to?

A

Lack of bacterium-free zone above the epithelium -> bacterial colonization of crypts -> colitis

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44
Q

What is the daily prodyuction of IgA in the intestine? How much % of the total immunoglobulin production is this?

A

3-5 grams of IgA/day, 75% of total production

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45
Q

What is the role of IgA in intestinal barrier functions?

A

Allows for selective colonization by bacteria, whilst preventing others from attaching

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46
Q

What triggers secretion of AMPs by Paneth cells?

A

TLR activation

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47
Q

What is the effect of a deletion of Paneth cells?

A

Disturbances of commensal bacteria, leading to more drainage of commensals to mesenteric lymph nodes

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48
Q

How do M-cells selectively take up antigens?

A

PRRs recognize relevant antigens

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49
Q

Which three mechanisms does the intestine have for antigen-uptake across the epithelium?

A
  1. Passive diffusion
  2. M-cells
  3. Macrophage uptake
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50
Q

How do macrophages take up antigens from the intestine?

A

Break tight junctions between epithelial cells and extend cytoplasm into the lumen to sample it

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51
Q

What is the effect of increased bacterial load on the number of macrophage protrusions in the intestinal epithelium?

A

Amount of macrophage protrusions increases

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52
Q

What are the epithelial barrier & antigen sampling characteristics of the small intestine? (4)

A
  1. Presence of M-cells
  2. Thin mucus layer
  3. Presence of Paneth cells
  4. Peyer’s patches
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53
Q

What are the epithelial barrier & antigen sampling characteristics of the colon? (4)

A
  1. Absence of M-cells
  2. Thick mucus layer
  3. Absence of Paneth cells
  4. Isolated lympoid follicles
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54
Q

How does a cell in the intestine determine whether to respond to PRR activation or not?

A

Specific combinations of PRR activation produces specific cocktails of inflammatory mediators, dictating responses

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55
Q

What are the two functions of NF-κB in the intestine?

A
  1. Production of inflammatory mediators upon activation of PRRs
  2. Intestinal epithelial homeostasis
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56
Q

By which factor is NF-κB inhibited?

A

IκB

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57
Q

How is IκB inactivated, allowing for the activation of NF-κB?

A

Phosphorylation of IκB allows it to be ubiquinated -> IκB broken down in proteasome, releasing NF-κB

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58
Q

What is the function of NF-κB in intestinal epithelial cells?

A

Necessary for epithelial cell survival

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59
Q

What is the effect of loss of NF-κB in intestinal epithelial cells?

A

Disrupted epithelial barrier function -> bacteria leak in -> macrophage activation -> chronic intestinal inflammation

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60
Q

What is the effect of NF-κB in macrophages? (3)

A
  1. Survival
  2. Pro-inflammatory factor expression
  3. Host defence
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61
Q

Where are most PRRs in the intestine located? Why there?

A

Basolateral side -> allows for sensing of bacterial tissue invasion, whilst not getting activated by intraluminal presence of bacteria

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62
Q

In which areas of the intestine are TLRs located on the apical side of epithelium?

A
  1. Close to Peyer’s patches
  2. Colon
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63
Q

True or false: small intestine & colon express the same TLRs

A

False; they express different TLRs because they have a different microbiological profile, requiring different receptor signatures

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64
Q

What is the effect of repetitive activation of PRRs by the same pathogen?

A

Desensitization of epithelium, leading to hyporesponsiveness for that pathogen

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65
Q

What are the homeostatic functions of resident macrophages in the intestine? (4)

A
  1. Elimination of invading commensal bacteria
  2. Maintenance of Tregs
  3. Phagocytosis of senescent and apoptotic epithelial cells
  4. Transfer of antigens to migratory DCs
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66
Q

What is the effect of activation of resident phagocytes by danger molecules?

A

Inflammatory response

67
Q

Which group of macrophages in the intestine is particularly prone to inflammatory reactions? Why?

A

Monocyte precursors from blood; these have not been conditioned for the gut environment and are hyperreactive against the antigens found there

68
Q

What are the functions of inflammatory macrophages/moncoytes in the intestine? (3)

A
  1. Increased phagocytosis -> elimination of invading pathogens
  2. Maintenance of pro-inflammatory effector T-cells
  3. Production of pro-inflammatory cytokines & chemokines
69
Q

What hampers mucosal vaccination of the intestine? How can this be overcome?

A

Predominant tolerance of the intestinal mucosa against mucosal signals; can be overcome by incorporating a strong danger signal in the intestine

70
Q

What is the function of DCs in the intestine? What characteristics do they have towards that end? (4)

A

Sampling of micro-environment and antigen presentation in mesenteric lymph nodes

  1. Limited phagocytosis
  2. Limited killing
  3. High antigen-presenting capacity
  4. High migration capacity
71
Q

What is the function of macrophages in the intestine? What characteristics do they have towards that end?

A

Important in homeostasis/governing responses in healthy tissue

  1. High phagocytosis
  2. High killing
  3. Low antigen-presenting capacity
  4. Low migration capacity
72
Q

What are markers of DCs in the intestine? Where are they located?

A

CD103+ cells in the lamina propria

73
Q

What are markers of macrophages in the intestine? Where are they located?

A

CD103- CX3CR1+ cells located under the epithelium

74
Q

The small intestine contains more [DCs than macrophages/macrophages than DCs]

A

More macrophages than DCs

75
Q

True or false: the intestine contains a lot of naïve cells

A

False; nearly all memory cells

76
Q

What happens when T-cells in the Peyer’s patch are activated?

A

Migration to lamina propria

77
Q

In which two ways can mesenteric lymphocytes be activated?

A
  1. DCs drain to mesenteric lymph nodes and present antigen to T-cells
  2. Free-floating antigens passively reach the lymph node, after which they are taken up by subcapsular macrophages/B-cells and presented to T-cells
78
Q

Where are subcapsular macrophages located in the lymph node?

A

Subcapsular space

79
Q

How to activated T-cells migrate back to the intestine?

A

T-cells undergo migration-dependent imprinting

80
Q

What is migration-dependent imprinting?

A

Induction of specific chemokine receptors & adhesion molecules due to instruction by DCs

81
Q

What is an important adhesion molecule for intestinal homing?

A

α4β7

82
Q

True or false: tolerance in the intestine is mainly the result of the immune system ignoring antigens

A

False; there are T-cell responses to almost all food proteins

83
Q

What is the effect of the presentation of food antigens by DCs in mesenteric lymph nodes & Peyer’s patches?

A

Induction of antigen-specific Tregs

84
Q

How long after encountering new food antigens are functional Tregs produced?

A

72 hours

85
Q

What is an important marker of many Tregs in the intestine?

A

FoxP3+

86
Q

How can tolerance to food antigens be overcome? Why does this overturn tolerance?

A

Cholera toxin -> strong danger signal

87
Q

Which factors contribute to a regulatory environment in the intestine? (3)

A
  1. CD103+ DCs
  2. Dietary vitamin A
  3. TGF-β
88
Q

What do CD103+ DCs do to dietary vitamin A?

A

Convert it to retinoic acid

89
Q

Which combination of DC-derived factors leads to the induction of Tregs in the intestine? (2)

A
  1. Retinoic from dietary vitamin A
  2. TGF-β
90
Q

What is the effect of the presence of retinoic acid + TGF-β on inducted Tregs? Why is this beneficial?

A
  1. Expression of CCR9
  2. Expression of α7β4

Both are homing factors needed to home into the small intestine

91
Q

Which cytokine is key in Treg function in the intestine?

A

IL-10

92
Q

How deep should an intestinal biopsy be to adequately be able to judge it? Why?

A

Until the muscularis mucosae; allows for orientation of the biopsy

93
Q

How many IELs should be visible in intestinal biopsies?

A

<20-25 IELs/100 epithelial cells

94
Q

What is the ratio of villi length:crypt depth in adults & children?

A

Adults: 3:1
Children: 2:1

95
Q

Based on which factors is celiac disease diagnosed? (5)

A
  1. Clinical manifestations
  2. Serological markers
  3. Genetic testing
  4. Response to gluten-free diet
  5. Histopathologic examination
96
Q

Is histopathologic examination performed in routine diagnostics of celiac disease?

A

No; only in children and borderline cases

97
Q

Why is early and correct diagnosis of celiac disease important? (2)

A
  1. Allows for initiation of gluten-free diet to avoid complications
  2. Allows for identification of non-celiac disease conditions
98
Q

From which sites do biopsies need to be taken in order to be able to diagnose celiac disease? (2)

A
  1. Duodenal bulb
  2. Distal part of duodenum
99
Q

What are two important biopsy prerequisities for accurate celiac disease diagnosis?

A
  1. Biopsy tissue fragments well-oriented
  2. Biopsies performed when patient was on gluten-containing diet
100
Q

What histological pattern can be observed in celiac disease? (3)

A
  1. Disruption of villi:crypt ratio
  2. Increased amounts of IELs
  3. Crypt hyperplasia
101
Q

In which way is the villi:crypt ratio disturbed in celiac disease?

A

Short villi (1:1) or no villi (mucosal flattening)

102
Q

What is the primary location of ulcerative colitis?

A

Primarily rectal & left-sided colitis

103
Q

Where in the digestive tract does Crohn’s disease occur? Where is it most frequently found?

A

All across the digestive tract; most frequently terminal ileum

104
Q

How is the diagnosis of IBD made? (4)

A
  1. Clinical manifestations
  2. Endoscopic findings
  3. Imaging features
  4. Microscopic features
105
Q

What is the role of the pathologist in IBD? (2)

A
  1. Assess distribution of disease
  2. Recognize chronic changes & acute inflammation due to IBD
106
Q

In which anatomical location is it most difficult to distinguish between ulcerative colitis & Crohn’s disease?

A

Colon -> both can occur there and look similar

107
Q

What are macroscopic features of Crohn’s disease? (3)

A
  1. Cobblestone aspect of the intestinal wall
  2. Strictures of the intestinal wall
  3. Ulcerations of the intestinal wall
108
Q

What are microscopic features of IBD in the colon? (4)

A
  1. Architectural changes
  2. Chronic inflammation of the lamina propria
  3. Acute inflammation
  4. Epithelial changes
109
Q

Which architectural changes can be observed in IBD in the colon? (2)

A
  1. Irregular/villiform mucosal surface
  2. Crypt distortion & atrophy (loss of crypts & shallow crypts)
110
Q

How can chronic inflammation of the lamina propria be seen in IBD? (2)

A
  1. Increase of non-aggregated plasma cells & lymphocytes in lamina propria
  2. Basal lymphoplasmacytosis
111
Q

Which presentations of acute inflammation can be seen in microscopy of the colon in IBD? (2)

A
  1. Formation of crypt abscesses/cryptitis due to neutrophilic inflammation
  2. Ulceration of the intestinal wall
112
Q

Which epithelial changes can be observed in colonic IBD? (2)

A
  1. Paneth cell metaplasia to the distal colon
  2. Mucin depletion of epithelial cells of the mucosa
113
Q

Which features can be used to distinguish CD from UC? (2)

A
  1. Presence of granulomas
  2. Presence of giant cells
114
Q

What are features of IBD in the small bowel? (3)

A
  1. Architectural disturbance
  2. Inflammatory component of the lamina propria
  3. Pyloric metaplasia
115
Q

What are causes of dysbiosis of the intestinal microbiome? (4)

A
  1. Host genetics
  2. Lifestyle
  3. Early colonization (bith in hospitals)
  4. Medical practices
116
Q

What is inflammatory bowel disease (definition)?

A

Inappropriate inflammatory response to intestinal microbes in a genetically susceptible host

117
Q

In which ways can immune responses in IBD be inappropriate? (2)

A
  1. Hyporesponsiveness
  2. Hyperresponsiveness
118
Q

Which kind of genetic alterations are mainly found in IBD?

A

SNPs

119
Q

In which locations is CD mainly found? (2)

A

Locations with high microbe diversity/numbers:
1. Terminal ileum
2. Colon

120
Q

What are histological aspects of Crohn’s disease? (5)

A
  1. Patchy
  2. Transmural
  3. Dense lymphocyte infiltration
  4. Granulomas in 60% of patients
  5. Ulcer formation
121
Q

What are histological aspects of ulcerative colitis? (4)

A
  1. Superficial layers affected
  2. Infiltration of lymphocytes & granulocytes
  3. Loss of goblet cells (empty)
  4. Presence of ulcerations & crypt abscesses
122
Q

Genes involved in which functions have been implicated in IBD? (5)

A
  1. Immune regulation
  2. Neutrophil function, phagocytosis & bacterial killing
  3. Innate immune activation
  4. Lymphocyte selection & FoxP3 Tregs
  5. Epithelial barrier/responses
123
Q

SNPs in which groups of genes are primarily associated with CD? (2)

A
  1. PRRs
  2. Cytokines
124
Q

SNPs in which groups of genes are primarily associated with UC? (2)

A
  1. Cytokines
  2. Epithelial barriers
125
Q

What are characteristics of IBD due to monogenic mutations?

A

Early onset and severe

126
Q

Why is studying monogenic IBD informative for the whole group of IBD?

A

It can reveal pathways involved in IBD

127
Q

Disruptions in the NOD2 pathway can lead to IBD. Does this lead to UC or CD?

A

CD

128
Q

What is the physiological function of NOD2?

A

PRR

129
Q

True or false: there are complete NOD2 insufficient patients

A

False; no complete NOD2 knockout has been found, but there are cases in which multiple SNPs severely hamper NOD2 function

130
Q

How does CD due to NOD2 deficiency respond to treatment?

A

Very treatment-resistant

131
Q

What are physiological functions of NOD2? (2)

A
  1. Maintenance of Paneth cells
  2. Physiology of APCs
132
Q

What is the function of NOD2 for Paneth cells?

A

Important for the production of AMPs, particularly cryptidin

133
Q

What is the effect of NOD2 disruption on APCs? (2)

A
  1. Increased killing
  2. Reduced TLR2 signaling -> reduced production of pro-inflammatory cytokines
134
Q

What is the effect of disruption of IL-10 signaling in the intestine?

A

Small intestinal & colonic severe early-onset IBD

135
Q

What is the effect of IL-10 deletion in Tregs in the small intestine (in mice)?

A

No effect -> other cells than Tregs are responsible for IL-10 production in the small intestine

136
Q

What is the effect of IL-10 deletion in Tregs in the colon (in mice)?

A

IBD -> Tregs are an essential source of IL-10 in the colon

137
Q

SNPs in which adaptive genes are mostly involved in IBD? (3)

A

Th1/Th17-function:
1. Innate cytokines involved in Th1/Th17 differentiation
2. Transcription factors of Th1/Th17 cells
3. T-cell derived cytokines

138
Q

Which cytokine is fundamental in CD?

A

IFN-γ

139
Q

Which cytokine is fundamental in UC?

A

IL-17

140
Q

What are the treatment goals of IBD-treatment? (2)

A
  1. Induce & maintain remission
  2. Avoid complications
141
Q

What is the initial phase of IBD treatment?

A

Strong immunosuppression using corticosteroids

142
Q

Which treatment strategies are available for IBD? (5)

A
  1. Exclusive enteral nutrition
  2. Corticosteroids
  3. Anti-inflammatory drugs
  4. Immunomodulators
  5. Biologicals aimed at involved cytokines
143
Q

True or false: exclucive enteral nutrition has (some) effect in all IBD patients

A

False; only works in a subgroup of patients

144
Q

Which anti-inflammatory drugs are used in the treatment of IBD? (2)

A
  1. Sulfasalazine (SASP)
  2. Mesalazine (5-ASA)
145
Q

Which immunomodulators are used in the treatment of IBD? (3)

A
  1. Methotrexate
  2. Tacrolimus
  3. Azathioprine
146
Q

What is the main cytokine targeted by cytokine treatments in IBD?

A

TNF-α

147
Q

What are proposed new options for IBD treatment? (4)

A
  1. Cytokine therapies against cytokines involved
  2. T-cell blocking therapies
  3. Therapies blocking cell recruitment
  4. Therapies blocking growth factors
148
Q

Which involved cytokines could be targeted in IBD, in addition to TNF-α? (3)

A
  1. IFN-γ
  2. IL-6
  3. IL-12
149
Q

What is gluten?

A

Protein component of many grains

150
Q

What is the function of gluten for grains?

A

Storage protein

151
Q

Gluten is [soluble/insoluble] in water

A

Insoluble

152
Q

What makes gluten hard to break down? (2)

A
  1. Disulfide & hydrogen bonds, forming tight aggregates
  2. Rich in proline
153
Q

What is coeliac disease (definition)?

A

Gluten-induced inflammation of the GI-tract

154
Q

What is the main effect of coeliac disease on the body?

A

Disturbed nutrient uptake

155
Q

What is the treatment of coeliac disease?

A

Gluten-free diet

156
Q

How many % of the Dutch population suffers from coeliac disease? How many of them are diagnosed?

A

~1% = 170.000 people, of which 25.000 are diagnosed -> lots of undiagnosed infections

157
Q

Which two HLA types can be present in coeliac disease? How many % has each?

A
  1. HLA-DQ2 = 95%
  2. HLA-DQ8 = 5%
158
Q

Which serum marker is used for the diagnosis of coeliac disease?

A

Anti-tissue transglutaminase IgA

159
Q

What is the physiological function of tissue transglutaminase?

A

Tissue repair

159
Q

The antibodies against TG2 in coeliac disease are [binding/neutralizing] antibodies

A

Binding antibodies

160
Q

Why is the presence of anti-TG2 antibodies alone insufficient for diagnosis of coeliac disease?

A

These could be transiently present in other diseases

161
Q

Which processes enable reactions to gluten in coeliac disease? (3)

A
  1. Gluten is degraded in the intestinal lumen and passes the epithelial barrier
  2. TG2 deaminates gliadin, changing its confirmation
  3. The changed confirmation of gliadin allows it to bind in HLA-DQ2/-DQ8, causing antigen presentation of T-cells
162
Q

Which adaptive responses are involved in coeliac disease? (2)

A
  1. Induction of gliadin-specific IFN-γ producing CD4+ T-cells by presentation of gluten on HLA
  2. Induction of a plasma cell response, leading to anti-TG2 antibodies
163
Q

Which innate responses are involved in coeliac disease? (3)

A
  1. Stress of epithelial cells leads to secretion of IL-15, leading to induction of IELs
  2. Stress of epithelial cells leads to NK-receptor ligand expression, resulting in killing of epithelial cells
  3. Killing of epithelial cells by cytotoxic CD8+ IELs
164
Q

What is the role of IL-15 in coeliac disease?

A

Leads to induction/activation of cytotoxic IELs that kill epithelial cells

165
Q

What causes epithelial flattening in coeliac disease?

A

Killing of stressed epithelial cells by NK-cells

166
Q

A large % of the population has susceptible HLA-types, yet only a small % has coeliac disease. What maintains balance in healthy individuals?

A

Tregs

167
Q

What kind of Tregs are necessary for the maintenance of tolerance to gluten? Which cytokine do they produce?

A

Tr1-like cells: FoxP3- IL-10 producing T-cells

168
Q

What is the effect of disrupted IL-10 function in coeliac disease? (2)

A
  1. IEL infiltration
  2. Crypt hyperplasia

I&I WC1 (20 decks)

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