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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
Th17 is beneficial against
extracellular bacteria and fungi
26
Th1 pathology=
chronic inflammation | autoimmunity
27
Th2 pathology=
allergy asthma
28
Th17 pathology=
chronic inflammation | autoimmunity
29
what 2 parts of GALT are there
- organised tissue | - scattered lymphoid cells
30
where does the immune response in GALT start
organised tissue = induction site
31
3 parts of the organised tissue in GALT
- peyer's patches - isolated lymphoid follicles - mesenteric lymph nodes
32
where are peyers patches
small intestine
33
where are isolated lymphoid follicles
small and large intestine
34
what is special about the mesenteric lymph node
largest LN in body
35
2 types of scattered lymphoid cells
- lamina propria leukocytes (LPL) | - intraepithelial lymphocytes (IEL)
36
what immune cells are in the lamina propria (5)
``` CD4+ CD8+ DCs plasma cells macrophages ```
37
what immune cells are in the epithelial layer of the gut
intraepithelial lymphocytes
38
what are intraepithelial lymphocytes
specialised types of T-cells mainly found in gut
39
before antigens can stimulate the mucosal immune system what must happen to them
they must be transported across the epithelial barrier
40
what epithelial cells cover peyers patches
specialized M cells
41
what other epithelium are M cell a part of
isolated lymphoid follicles
42
how do M cells take up antigens
by endocytosis and phagocytosis
43
what happens to antigens when they are released from the basal surface of M cells
the antigen is bound to dendritic cells which activate T cells
44
what happens to antigen loaded DCs
migrate to T-cell areas of PP and to mesenteric lymph nodes to activate T-cells
45
e.g 4 pathogens which target M cells to access the subepithelial space
polio retroviruses salmonella shigella
46
what cells can capture antigens from intestinal lumen
macrophages
47
when macrophages have captured antigen what do they do
hand over Ag to DCs in lamina propria
48
what happens to DCs in a healthy intestine
they become conditioned
49
what is DC conditioning
to make DCs favour the induction of Treg response
50
what can microbial metabolites do in the gut
control the immune response
51
how do microbial metabolites control the immune response
via short chain fatty acids
52
what do short chain fatty acids from microbes do
- instruct naive T-cells to become T-reg | - dampen innate immune response
53
name 3 Treg cells
Tr1 Th3 CD25
54
2 ways intestinal homeostasis can become unbalanced causing inflammation
- too many T effector cells | - too little T regulatory cells
55
dominant antibody in the mucosal immune system
IgA
56
type of IgA in blood
monomeric
57
type of IgA in mucosal tissue
dimeric IgA linked by J chain
58
how much IgA produced each day
5g
59
where is IgA transported into the gut lumen
epithelial cells at the base of crypts
60
what transport protein moves IgA into the gut lumen
poly-Ig receptor
61
what happens to part of the poly-Ig receptor
part of the receptor remains associated with IgA known as the secretory component
62
where does IgA bind in the gut lumen
the layer of mucus overlying the gut epithelium (via its secretory component)
63
functions of secretory IgA
- neutralizes toxins, enzymes and LPS | - prevents adherence of microorganisms
64
what does IgA have little capacity for
activation of classical complement and cannot induce inflammation
65
main overall function of IgA
limit access of pathogens to mucosal surfaces, without risking inflammation
66
what happens in IgA deficient patients
IgM replaces IgA in mucosal secretions
67
2 harmless antigens the immune system needs to ignore
food | commensal
68
how are food antigens ignored
- specific peripheral unresponsiveness (oral tolerance) - antigen specific effect Tcells turned off - antigen specific Treg generated
69
how are commensals ignored
induce IgA and Treg in intestine
70
how does the gut mount an immune response to pathogens
- in presence of pathogens DCs become fully activated and induce CD4+ T-cells to become effectors - innate immune system activated via pattern- recognition
71
what does TLR4 recognise
LPS
72
what does TLR5 recognise
flagellin
73
what does TLR2 recognise
peptidoglycan
74
what does DC maturation lead to
- up-regulation of MHC and co-stimulatory molecules | - cytokine production
75
how come only invading pathogens can trigger TLR activation
- TLR4 is only expressed in crypt base epithelial cells | - TLR5 only expressed basolaterally
76
how do commensals avoid PRR activation
changes in flagelling sequence to make TLR5 hypo responsive
77
what does salmonella type 3 secretions system cause
activation of intracellular inflammasome
78
symbiosis=
co-evolution between commensals and their host
79
regulatory T-cell response releases
IL-10 | TGF-beta
80
effector T cell response=
Th1/Th17 --> IFN gamma + IL-17
81
what is celiac disease
inappropriate immune response to gluten
82
2 mutations in IBD associated with antibacterial immune responses
NOD2 | IL-23
83
where is NOD2 gene found
paneth cells of gut | innate immune cells
84
how is NOD2 stimulated
by peptidoglycan (Gr+and Gr-)
85
what does NOD2 stimulation lead to
production of anti-microbials
86
when is IL-23 produced
by innate cells following PRR
87
4 types of drugs used to treat IBD
aminosalicylates corticosteroids immunosuppressants biologicals
88
e.g of 2 aminosalicylates
sulphasalazine | mesalazine
89
what do aminosalicylates do
dampen inflammation
90
3 corticosteroids
prednisolone prednisone hydrocortisone
91
2 immunosuppressants
azathioprine | methotrexate
92
2 biologicals
Infliximab | adalimumab
93
MOA of infliximab and adalimumab
anti-TNF alpha monoclonal antibodies

Block 15 Ellen (11 decks)

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