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PBL SEM 4 > immunology of the gut > Flashcards

immunology of the gut Flashcards

1
Q

the GIT has an undulating surface which increases SA for ______ and ______

A

absorption and secretion

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2
Q

what kind of epithelium?

A

simple columnar

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3
Q

what are the functions of mucus secreted by goblet cells?

A
  • lubricant
  • prevents mechanical stress on epithelium
  • thick layer provide stable micro environment
  • prevents invasion
  • essential environment for micro flora
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4
Q

in a bad E.coli outbreak, what did some people go on to develop?

A

rare haemolytic uraemic syndrome

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5
Q

enteroaggregative strain of E.coli had acquired what?

A

Shiga toxin which causes haemolytic uraemic syndrome — the toxic could get through the mucus layer

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6
Q

muslce in the stomach?

A

3 layers to churn food — longitudinal, circular, oblique

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7
Q

what does the low pH of the stomach enable?

A

pepsin to degrade protein

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8
Q

describe gastrin epithelium

A

columnar epithelium with gastric pits — with gastric glands - help maintain acidic pH

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9
Q

what is the connective tissue layer in the stomach?

A

serosa

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10
Q

how is gastric epithelium protected from the acidic pH?

A

specialised epithelial cells secrete bicarbonate

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11
Q

what are the 4 key pathogenic characteristics of H.pylori?

A
  1. flagelli so can swim through thick mucus layer
  2. urease to neutralise gastric acid — creates neutral environment around itself
  3. proliferate
  4. mucinase to degrade mucus, allowing acid to cause the inflammation — gastric ulcer
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12
Q

what is the strongest known risk factor for gastric cancer?

A

infection wit H pylori

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13
Q

what is in the upper layer of mucus?

A

colonised by bacteria

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14
Q

what does the absence of gut bacteria affect?

A
  • behaviour
  • gut homeostasis
  • immune response under stress
  • body weight
  • brain development and gene expression
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15
Q

describe antibiotics, C.difficile infection and faecal transplant theory

A
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16
Q

what is clostridium difficile?

A

a spore-forming gram positive bacillus which is part of normal healthy flora in 4% of healthy individuals

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17
Q

what are the most severe symptoms of a clostridium difficile infection? (it is a spectrum from this to asymptomatic)

A
  • severe diarrhoea
  • severe abdominal pain
  • white blood cell count > 15000 cells/ul
  • toxic megacolon
  • organ failure
  • mortality rate 35-80%
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18
Q

what are examples of antimicrobial peptides?

A

a and b defensins

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19
Q

what are a and b defensins secreted by?

A

paneth cells

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20
Q

where are paneth cells located?

A

base of crypt in SI

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21
Q

there is good experimental evidence that gut bacteria maintain homeostasis how?

A

by actually stimulating the secretion of antimicrobial peptides

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22
Q

what is a GI specific antibody responsible for primary defence against bacteria?

A

IgA

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23
Q

describe SIgA

A
  • dimer
  • secreted by plasma cells (mature differentiated B cells)
  • enter lumen by active transport
  • 1/700 people dont have sIgA
  • most common immune deficiencies in europe
  • antigen and T cell independent
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24
Q

what does SIgA seem to have some specificity for in the gut?

A

pathogenic bacteria — binds to all the stuff that cause colitis

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25
Q

what are the 3 natural defences in the gut?

A

mucus, micro biome and antibody

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26
Q

what are located between paneth cells?

A

pluripotent stem cells

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27
Q

what cells in the intestinal epithelium are responsible for opioid release?

A

tuft cells

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28
Q

what cells in the GIT are responsible for nutrients absoprtion?

A

enterocytes

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29
Q

a group of well-organized lymphoid follicles located in the_________ and ___________ of the distal portion of the small intestine - the ileum and jejunum and sometimes in the duodenum

what is this describing?

A

a group of well-organized lymphoid follicles located in the lamina propria and submucosa of the distal portion of the small intestine - the ileum and jejunum and sometimes in the duodenum

Peyer’s patch

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30
Q

what happens to the stem cells?

A

move up from base of crypt as they proliferate and differentiate, then slough off at top

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31
Q

what enable the stem cells to remain sterile?

A

paneth cells

32
Q
A
33
Q

coeliac disease and villi

A
34
Q

intestinal dendritic cells vs macrophages

A

dendritic cells:
- migratory
- excellent primers of T cells via antigen presentation
- discrete subsets with different functions
- CD11b+/- CD103+/-
- derive from committed progenitor
- sample luminal bacteria - hard to find evidence

macrophages:
- non-migratory
- express CD64, CD11b, CD11c, CX3CR1
- replenished by blood monocytes
- phagocytes
- sample luminal bacteria?

35
Q

what are the front line cells for any bacteria trying to get through?

A

resident macrophages

36
Q

in mice, what macrophages control translocation of luminal bacteria to the draining lymph node?

A

CX3CR1+

37
Q

name 2 Th1 cells

A

IFN-y and TNF-a

38
Q

Th1 function

A

defence against intracellular parasites

39
Q

name 4 Th2 cells

A

IL-4/5/6/13

40
Q

Th2 function

A

allergy, asthma, controls parasites and extracelllar pathogens

41
Q

name 4 Th17 cells

A

IL-17A/17F/21/22

42
Q

Th17 functions

A

defence against pathogens, autoimmunity, transplantation rejection and cancer

43
Q

name 2 Treg cells

A

TGFB, Il-10

44
Q

Treg functions

A

immune homeostasis and maintains tolerance

45
Q

name a Tfh cell

A

CXCR5

= T follicular helper cell

46
Q

Tfh cell functions

A

help germinal centre B cells to make antibodies, affinity maturation and antibody class switching

47
Q

what differentiates in the different T cells?

A

naive CD4+ T cell

48
Q

what factors differentiate naive CD4+ T cell into Th1/2/17/reg/fh cells?

A
  1. IFN-y and IL-12 —> Th1
  2. IL-4 —> Th2
  3. TGFB and IL-6 —> Th17
  4. TGFb —> Treg
  5. IL-6 and IL-21 —> Tfh
49
Q

describe ILCs

A

= innate lymphoid cells

  • derived from common lymphoid progenitor
  • rely on IL2R signalling (as do T cells)
  • INNATE lymphocytes ie no T cell receptor
  • stimulated by cytokines or microbes (probably indirectly)
  • present at very low numbers in steady state (therefore hard to study)
  • characterised as ILC1, 2 or 3
  • mirror T cell differentiation patterns
50
Q

describe ILC1

A
  • IFNy producers
  • includes NK cells
  • express T-bet
51
Q

describe ILC2

A
  • IL5/IL13 produces
  • express RORa/GATA3
  • seen in allergy
  • respond to IL25/IL33
  • also called nuocytes, natural helper cells
52
Q

describe ILC3

A
  • IL17A and F / IL22 producers (may be IFNy)
  • express RORyt
  • respond to IL23
  • important in foetal lymphoid organogenesis
  • important in GALT formation
  • important in mucosal homeostasis
  • loss of ILC3 has been associated with HIV+ progression to AIDS
53
Q

ILC1/ILC2/ILC3 and NK cells frequency in colorectal cancer?

A

ILC1 ILC2 NK cells = increased frequency

ILC3 = decreased frequency = very bad for gut health = lose help to keep barrier intact

54
Q

what 2 things ‘keep everything happy’ (esp ILC3) in gut homeostasis?

A

IL-10 and TGF-B = Treg cells

Treg cells put a brake on inflammation

55
Q

what do dendritic cells do if there is an insult?

A

trigger production of inflammatory cytokines — drive inflammation

— need regulatory cytokines to resolve inflammation once pathogen gone

56
Q

what cell surface receptors put a brake on inflammation?

A

PD-1/PD-L1

CTLA4/B71 or 2

57
Q

CTLA4/B7 interaction between T cell and antigen presenting cell has what affect?

A

stops T cell activation

58
Q

interaction between T cell and dendritic cell requires what 3 signals?

A
  1. cytokine signal
  2. T cell receptor and MHC
  3. CD28
59
Q

what affect does PD-1/PD-L1 interaction have?

A

reduces T cell activation

60
Q

PD-1 is an immune ______ molecule to avoid _______

A
  • suppressive
  • over-activation
61
Q

where are PD-1 and PD-L1 expressed?

A
  1. infected cells — prevents efficient immunity to virally infected cells
  2. APCs and tissue — prevents immune recognition of self
  3. tumour cells — tumour evasion mechanism
62
Q

in non-IBD patients, colorectal cancer usual;lymph begins as what?

A

a non-cancerous (or benign) polyp

63
Q

what is a polyp?

A
  • a growth inside the colon or rectum that is not normal
  • can be several types
  • is not always cancerous
64
Q

what is seen in colorectal cancer in terms of epithelial cells?

A
  1. decreased epithelial cell turnover
  2. overgrowth of cells on epithelial lining of gut

malignant stem cells —> adenoma formation

65
Q

what are the chances of developing CRC for a man and women in their lifetime?

A

a man has a 1/17 chance, woman has a 1/18 chance

66
Q

in most people, how does sCRC develop?

A

slowly over a period of several years (10-20 years)

67
Q

what does an inflammatory micro environment promote?

A

tumourigenesis

68
Q

what is the biggest risk factor for CRC?

A

inflammation

69
Q

what is loss of barrier function possibly due to?

A

loss of ILCs due to chronic inflammation or dysbiosis (gut bacteria releasing toxins which damage the barrier and mucus)

70
Q

what happens when mucosal homeostasis is lost?

A

inflammatory bowel disease
- ulcerative colitis (tends to start in rectum)
- crohn’s disease (can be anywhere in GIT)

71
Q

what pathological things happen i. Crohn’s disease?

A
  • barrier defects : tight junction dysfunction
  • defective neutrophil function
  • paneth cell defects : reduces secretion of HD5
  • defective cell migration
  • effector T cell / T reg imbalance
  • paneth cell defects : NOD2 polymorphisms potentially affecting microbiome and response to commensal flora

DYSREGUALTION OF HOST FLORA CONTRIBUTES TO DISEASE

72
Q

having IBD and type 2 diabetes are risk factors for what?

A

colorectal cancer

73
Q

what is the overall increased risk of CRC for someone with IBD?

A

10-15%

74
Q

by how much does having a personal history of type 2 diabetes increase your risk of having CRC and colorectal polyps?

A

50%

75
Q

describe the intrinsic pathway to inflammation in tumour cells

A
  • normal tissue homeostasis disrupted
  • sequential mutations (prob in stem cell compartment)
  • epigenetic alterations
  • oxidative stress (Bcl2, p53)
  • proliferation / apoptosis dysregualtion
  • tumour progression
76
Q

describe the extrinsic pathway driven by chronic inflammation (eg IBD, dysbiosis)

A
  • inflammatory tumour micro environment
  • inflammatory cytokines (TNFa, IFNy, IL1)
  • reduced regulatory cytokines (IL10, TGFb)
  • disrupted homeostasis
  • proliferation / apoptosis dysregulation
  • tumour progression

PBL SEM 4 (50 decks)

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