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Block 15 Ellen > L3: Immunology of the gut > Flashcards

L3: Immunology of the gut Flashcards

1
Q

what property of mucosal surfaces makes them more susceptible to invasion by pathogens

A

thin and permeable barriers

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2
Q

3 protections against infection in the gut

A

epithelial tight junctions
goblet cells secrete mucins
-paneth cells secrete antimicrobial peptides

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3
Q

how many cells layers between bacteria and gut lumen

A

1 layer of epithelial cells

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4
Q

what is NALT

A

nasal associated lymphoid tissue

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5
Q

what is BALT

A

bronchus associated lymphoid tissue

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6
Q

what is GALT

A

gut associated lymphoid tissue

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7
Q

as you go down the GI tract what do the bacteria become

A

more anaerobic

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8
Q

2 tasks of mucosal immune system

A

ignore harmless antigens

mount protective immune response to pathogens

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9
Q

2 things that can go wrong in the gut immune system

A

celiac disease

IBD

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10
Q

cells of the innate immune response (4)

A

dendritic cells
macrophages
monocytes
granulocytes (neutrophils, eosinophils, basophils)

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11
Q

cells of the adaptive immune response

A

CD4+
CD8+
B-cells

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12
Q

how does the innate system recognise antigens

A

pattern recognition receptors

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13
Q

how does the adaptive immune system recognise pathogens

A

antigen- specific receptors

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14
Q

e.g of pattern recognition receptors

A

Toll-like receptors (TLRs), NODs/ CARDs

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15
Q

what do pattern recognition receptors recognise

A

pattern motifs like LPS and peptidoglycan

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16
Q

TCR recognises

A

peptide/ MHC complex

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17
Q

B-cell receptor recognises

A

ig antibody

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18
Q

what is the B-cell receptor the same as

A

the antibody it will secrete

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19
Q

3 effector T-cell subsets

A

Th1
Th2
Th17

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20
Q

Th1 releases –>

A

IFN gamma

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21
Q

Th2 releases –>

A

IL4

IL5

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22
Q

Th17 releases

A

IL17

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23
Q

Th1 is beneficial against

A

intracellular pathogens

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24
Q

Th2 is beneficial against

A

extracellular pathogens

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25
Q

Th17 is beneficial against

A

extracellular bacteria and fungi

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26
Q

Th1 pathology=

A

chronic inflammation

autoimmunity

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27
Q

Th2 pathology=

A

allergy asthma

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28
Q

Th17 pathology=

A

chronic inflammation

autoimmunity

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29
Q

what 2 parts of GALT are there

A
  • organised tissue

- scattered lymphoid cells

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30
Q

where does the immune response in GALT start

A

organised tissue = induction site

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31
Q

3 parts of the organised tissue in GALT

A
  • peyer’s patches
  • isolated lymphoid follicles
  • mesenteric lymph nodes
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32
Q

where are peyers patches

A

small intestine

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33
Q

where are isolated lymphoid follicles

A

small and large intestine

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34
Q

what is special about the mesenteric lymph node

A

largest LN in body

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35
Q

2 types of scattered lymphoid cells

A
  • lamina propria leukocytes (LPL)

- intraepithelial lymphocytes (IEL)

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36
Q

what immune cells are in the lamina propria (5)

A 
CD4+ 
CD8+
DCs 
plasma cells 
macrophages
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37
Q

what immune cells are in the epithelial layer of the gut

A

intraepithelial lymphocytes

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38
Q

what are intraepithelial lymphocytes

A

specialised types of T-cells mainly found in gut

39
Q

before antigens can stimulate the mucosal immune system what must happen to them

A

they must be transported across the epithelial barrier

40
Q

what epithelial cells cover peyers patches

A

specialized M cells

41
Q

what other epithelium are M cell a part of

A

isolated lymphoid follicles

42
Q

how do M cells take up antigens

A

by endocytosis and phagocytosis

43
Q

what happens to antigens when they are released from the basal surface of M cells

A

the antigen is bound to dendritic cells which activate T cells

44
Q

what happens to antigen loaded DCs

A

migrate to T-cell areas of PP and to mesenteric lymph nodes to activate T-cells

45
Q

e.g 4 pathogens which target M cells to access the subepithelial space

A

polio
retroviruses
salmonella
shigella

46
Q

what cells can capture antigens from intestinal lumen

A

macrophages

47
Q

when macrophages have captured antigen what do they do

A

hand over Ag to DCs in lamina propria

48
Q

what happens to DCs in a healthy intestine

A

they become conditioned

49
Q

what is DC conditioning

A

to make DCs favour the induction of Treg response

50
Q

what can microbial metabolites do in the gut

A

control the immune response

51
Q

how do microbial metabolites control the immune response

A

via short chain fatty acids

52
Q

what do short chain fatty acids from microbes do

A
  • instruct naive T-cells to become T-reg

- dampen innate immune response

53
Q

name 3 Treg cells

A

Tr1
Th3
CD25

54
Q

2 ways intestinal homeostasis can become unbalanced causing inflammation

A
  • too many T effector cells

- too little T regulatory cells

55
Q

dominant antibody in the mucosal immune system

A

IgA

56
Q

type of IgA in blood

A

monomeric

57
Q

type of IgA in mucosal tissue

A

dimeric IgA linked by J chain

58
Q

how much IgA produced each day

A

5g

59
Q

where is IgA transported into the gut lumen

A

epithelial cells at the base of crypts

60
Q

what transport protein moves IgA into the gut lumen

A

poly-Ig receptor

61
Q

what happens to part of the poly-Ig receptor

A

part of the receptor remains associated with IgA known as the secretory component

62
Q

where does IgA bind in the gut lumen

A

the layer of mucus overlying the gut epithelium (via its secretory component)

63
Q

functions of secretory IgA

A
  • neutralizes toxins, enzymes and LPS

- prevents adherence of microorganisms

64
Q

what does IgA have little capacity for

A

activation of classical complement and cannot induce inflammation

65
Q

main overall function of IgA

A

limit access of pathogens to mucosal surfaces, without risking inflammation

66
Q

what happens in IgA deficient patients

A

IgM replaces IgA in mucosal secretions

67
Q

2 harmless antigens the immune system needs to ignore

A

food

commensal

68
Q

how are food antigens ignored

A
  • specific peripheral unresponsiveness (oral tolerance)
  • antigen specific effect Tcells turned off
  • antigen specific Treg generated
69
Q

how are commensals ignored

A

induce IgA and Treg in intestine

70
Q

how does the gut mount an immune response to pathogens

A
  • in presence of pathogens DCs become fully activated and induce CD4+ T-cells to become effectors
  • innate immune system activated via pattern- recognition
71
Q

what does TLR4 recognise

A

LPS

72
Q

what does TLR5 recognise

A

flagellin

73
Q

what does TLR2 recognise

A

peptidoglycan

74
Q

what does DC maturation lead to

A
  • up-regulation of MHC and co-stimulatory molecules

- cytokine production

75
Q

how come only invading pathogens can trigger TLR activation

A
  • TLR4 is only expressed in crypt base epithelial cells

- TLR5 only expressed basolaterally

76
Q

how do commensals avoid PRR activation

A

changes in flagelling sequence to make TLR5 hypo responsive

77
Q

what does salmonella type 3 secretions system cause

A

activation of intracellular inflammasome

78
Q

symbiosis=

A

co-evolution between commensals and their host

79
Q

regulatory T-cell response releases

A

IL-10

TGF-beta

80
Q

effector T cell response=

A

Th1/Th17 –> IFN gamma + IL-17

81
Q

what is celiac disease

A

inappropriate immune response to gluten

82
Q

2 mutations in IBD associated with antibacterial immune responses

A

NOD2

IL-23

83
Q

where is NOD2 gene found

A

paneth cells of gut

innate immune cells

84
Q

how is NOD2 stimulated

A

by peptidoglycan (Gr+and Gr-)

85
Q

what does NOD2 stimulation lead to

A

production of anti-microbials

86
Q

when is IL-23 produced

A

by innate cells following PRR

87
Q

4 types of drugs used to treat IBD

A

aminosalicylates
corticosteroids
immunosuppressants
biologicals

88
Q

e.g of 2 aminosalicylates

A

sulphasalazine

mesalazine

89
Q

what do aminosalicylates do

A

dampen inflammation

90
Q

3 corticosteroids

A

prednisolone
prednisone
hydrocortisone

91
Q

2 immunosuppressants

A

azathioprine

methotrexate

92
Q

2 biologicals

A

Infliximab

adalimumab

93
Q

MOA of infliximab and adalimumab

A

anti-TNF alpha monoclonal antibodies

Block 15 Ellen (11 decks)

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