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Immunology - Test 3 AH > Chapter 14 - GI Immunity > Flashcards

Chapter 14 - GI Immunity Flashcards

0
Q

What has a multilayer epithelial barrier?

A

oral cavity and vagina

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1
Q

What immune system is the largest?

how many lymphocytes does it have?

A

GI

50 x 10^9

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2
Q

what utilizes M cells?

A

GI, tonsils, adenoids

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3
Q

Where do DCs travel to to present Ag to naive T cells?

A

draining LN

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4
Q

what happens at GALT sites

A

adaptive immune responses specialized for the particular mucosa are initiated

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5
Q

what happens to effector lymphocytes generated in LN or GALT?

A

enter the blood and home back to same organ

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6
Q

where are M cells present?

gamma delta T cells?

A

gut

epithelia

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7
Q

what specialized cells are restricted to 1 or more regional immune systems but not present throughout?

A

M cells
gamma delta T cells
subsets of IgA producing B cells
plasma cells

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8
Q

what are regional immune systems important for?

A

regulatory functions that prevent unwanted responses to nonpathogenic microbes and foreign substances

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9
Q

where is the number of microflora the highest, small or large intestine?

A

large intestine

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10
Q

what is the lamina propria?

A

under the epithelium, loose CT in the gut

contains blood and lymphatic vessels, MALT

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11
Q

what are the function of commensals (microflora)?

A

degradation of dietary components we cannot digest

compete with pathogenic microbes in the gut to prevent harmful infections

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12
Q

how can commensal organisms become lethal?

A

if they cross the mucosal barrier

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13
Q

what are the 2 forms of innate immune protection

A

physical and chemical

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14
Q

what are the physical barriers?

A

mucosal epithelial cells held together by tight junctions and their mucous secretions

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15
Q

what are the chemical barriers

A

anti-microbial peptide defensins

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16
Q

what is present in the lamina propria which can induce inflammation?

A

DCs, Macrophages, neutrophils

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17
Q

what do mucins do?

what do they include?

A

prevent microbes from contacting epithelial cells

secreted and cell surface glycoproteins

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18
Q

what are the layers of mucins?

A

outer less-dense layer with bacteria

dense inner layer that is bacteria free

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19
Q

the apical surface of GI epithelial cells is coated with what?

A

membrane-bound mucin proteins called the glycocalyx

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20
Q

what does the glycocalyx do?

A

physical barrier to prevent microbial contact

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21
Q

how and by what are mucins produced?

A

constitutively by epithelial cells and submucosal glands

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22
Q

how often are mucins replaced?

A

every 6-12 hours

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23
Q

what cytokines increase mucin production during inflammation?

A

IL-1, IL-4, IL-6, TNF, IFN-alpha, elastase, microbial adhesive proteins

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24
Q

What do inflammatory molecules do?

A

inc. mucin production and alter their glycosylation which inc. barrier function against pathogens

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25
Q

what do epithelial and Paneth cells produce?

for what

A

defensins constitutively

to provide innate immunity protection against luminal bacteria

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26
Q

how do defensins work?

A

exert lethal toxic effects on microbes by inserting into and causing loss of integrity of their outer phospholipid membranes

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27
Q

what are the major defensins in the small bowel?

colon?

A

alpha-defensins made by Paneths

beta-defensins made by epithelial

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28
Q

what are defects in defensin linked to?

A

Crohn’s disease

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29
Q

What are TLRs and NLRs expressed by for what?

A

intestinal epithelial cells to promote immune responses to invasive pathogens

limit inflammatory responses to microflora

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30
Q

what may microflora express?

A

lipopolysaccharide (-)
peptidoglycans (+)
CpG DNA
flagellin

31
Q

what do functional responses to TLR signaling do?

A

increase barrier function, not inflammation

32
Q

TLR5 recognizes what?

expressed where?

A

flagellin

basolateral surface

33
Q

where is NLR for flagellin expressed?

A

cytosol of intestinal epithelial cells

inflammatory response activated only when microbe enters cytosol

34
Q

how is adaptive immune response initiated?

A

APC with mucosal epithelial cells and lymphocytes

35
Q

what is the pathway of Ag delivery from lumen to GALT?

what is major form?

A

M cells

humoral immunity

36
Q

what does the dominant, cell-mediated immune response consist of?

what can control responses in the gut?

A

Th 17 cells

Treg cells

37
Q

what are the characteristics of M cells and what do they do?

A

have shorter villi, engage in transport of intact microbes or molecules across the mucosal barrier into GALT where they hand off to DC

38
Q

how are DCs in GALT induced and what do they convert

A

thymic stromal lymphopoietin (TSLP)

Vit A to Retinoic acid

39
Q

what are naive B or T cells exposed to retinoic acid and activated by Ag, induced expression of what occurs?

A

CCR9 and intergrin alpha4-beta7 on plasma cells and effector T cells

40
Q

what causes effector lymphocytes to enter circulation and home back into the gut lamina propria?

A

CCL25 and MadCAM displayed on lamina propria endothelial cells

41
Q

in T-dependent IgA class switching, where do DCs capture Ags delivered by M cells and where do they migrate to?

A

subepithelial dome of Peyer’s patches

migrate to interfollicular zone where they present Ag to naive CD4 T cells

42
Q

what do the activated T cells differentiate into?

A

Th cells with a T follicular helper phenotype

43
Q

what is B cell class switching to IgA stimulated through?

what does TD pathway yield?

A

CD40L binding to B cell CD40 with TGF-Beta

high affinity IgA Abs

44
Q

what does T-independent IgA class switching involve?

what does this pathway yield?

A

B-1 cells, DC secrete BAFF, APRIL, and TGF-Beta which induces the switch

low affinity IgA Ab

45
Q

what does IgA produced in the lamina propria bind to?

how is it released into lumen

A

poly-Ig receptor

proteolytic cleavage

46
Q

what is the lamina propria of the small bowel rich in?

where are there no Th17 cells?

A

Il-17 producing cells

colon

47
Q

what is the function of Th 17 cells?

what cytokines does it produce?

A

maintains mucosal epithelial barrier

IL-17 and IL-22

48
Q

what do IL-17 and IL-22 act on?

function?

A

intestinal epithelial cells, induce expression of mucins and Beta-defensins

protect the epithelial cells against microbe-induced injury

49
Q

what is abundant in GALT, what do these cells do?

A

Treg, prevent inflammatory reactions against intestinal commensal microbes

50
Q

what factors contribute to the generation of Treg cells in the GI?

how do these cells suppress immune responses?

A

DCs
retinoic acid (promotes FoxP3)
TGF-Beta (promotes FoxP3)

production of IL-10

51
Q

what cytokines are important for homeostasis?

what do deficiencies of these result in?

A

TGF-Beta, IL-10, and IL-2

pathological bowel inflammation

52
Q

what is associated with colitis in children?

A

mutation in IL-10 and IL-10R

53
Q

what does a defect in IL-2 or IL-2R lead to?

A

IBD, due to defect of development of Treg cells

54
Q

what mechanisms of oral tolerance are there?

A

anergy
deletion
Treg-mediated suppression

55
Q

what % of T cells in GALT are Treg cells?

A

10%

56
Q

what are PAMPs and TLRs they bind on epithelial cells needed for?

A

proliferation and repair of the intestinal barrier after injury

57
Q

what do microflora stimulate?

A

mucins and anti-microbial peptides that prevent gram(+) bacterial colonization

58
Q

what do short-chain FAs from gut do?

peptidoglycycan from commercials?

A

dampen neutrophil inflammatory response

enhances ability of circulating neutrophils to kill gram(+) bacteria

59
Q

what is microflora required for?

A

systemic anti-viral functions of macrophages, DCs, and NK cells

60
Q

IgA production is dependent on what?

what do commensal organisms induce?

A

luminal flora

IgA switch factors (BAFF, APRIL, retinoic acid)

61
Q

what does IgA in the gut do?

A

reduce innate response to commensals

limits B cell activation and Ab responses to other isotypes

62
Q

what do dietary products do?

A

shape the microbial community

63
Q

what do microbiota do?

A

change the nutritional value of the consumed food

64
Q

what happens to unmodified dietary components?

A

absorbed in the intestine, interact with immune cells

65
Q

what does MAMP/PAMP signaling via TLR do?

A

modifies local mucosal immunity

66
Q

what does microbe-modified dietary components (ex. acetate)

A

stimulate IL-10 production regulating metabolic activities in the lamina propria

67
Q

what are the 2 main types of IBD?

A

Crohn’s - affects entire thickness, involves terminal ileum

ulcerative colitis - patchy damage, restricted to colonic mucosa

68
Q

what are treatments of IBD?

A

anti-inflammatories

sulfasalazine, corticosteroids, TNF antagonists, and antimetabolites

69
Q

Defects in innate immunity to gut commensals

A

defective expression of defensins –> increased commensal invasion

inadequate negative regulation

70
Q

what is Crohn’s characterized by?

A

granulomatous inflammation drive by IFN-gamma producing Th1 cells

71
Q

what are possible causes of IBD?

A

inadequate Treg-mediated suppression

absence or depletion of Treg

IL-2, IL-2R, FoxP3 mutation

72
Q

what causes IPEX?

symptoms?

A

FoxP3 mutation

severe gut inflammation

73
Q

what are the 2 alleles people with Celiac have?

what type of cells involved in the pathogenesis?

A

HLA-DQ2 and HLA-DQ8

CD4 T

74
Q

what does cross-linking and deamindation of gluten peptides?

A

transglutaminase 2 (TG2)

75
Q

what releases MMPs?

what is the result?

A

myofibroblasts

mucosal remodeling and villus atrophy

76
Q

what does IL-15 do?

A

links adaptive immune system to innate immune response

Immunology - Test 3 AH (6 decks)

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