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GI > Mucosal Immunity > Flashcards

Mucosal Immunity Flashcards

1
Q

what are the 4 physiological functions of mucosal tissue?

A
  • gas exchange
  • food absorption
  • sensory activities
  • reproduction
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2
Q

why id the mucosal tissue highly vulnerable?

What does trans and paracellular transport mean?

A

= due to fragility and permeability

Trans - through cells
Para - in tight junctions

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3
Q

what feature of a lymph node brings the antigen into the lymph node?

A

= afferent lymphatic vessels

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4
Q

what feature of a lymph nodes causes the antigens to leave the lymph nodes?

A

= efferent lymphatic vessels

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5
Q

describe 3 anatomical features of gut mucosal immune system?

A

1) intimate relationship between mucosal epithelial and lymphoid tissue
2) organised lymphoid tissue structure unique to mucosal site
3) specialised antigen uptake mechanism

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6
Q

what are the effector mechanisms used in the GUT?

A
  • activated/memory T cells

- effector/regulatory T cells

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7
Q

describe the immuno-regulatory environment of the gut.

A
  • down regulation of immune response

- inhibitory macrophages and tolerating dendritic cells

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8
Q

where are intestinal lymphocytes found?

A

= in organised tissue where immune responses are induced, and scattered throughout the intestine, where they carry out effecter functions.

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9
Q

what are Peyer’s patched covered by?

A

= an epithelial layer containing specialised cells called M cells which have characteristic membrane ruffles.

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10
Q

why does the M cells have ruffles one the membrane?

A

increase the surface area

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11
Q

what shape do Peyers patches form? and what colour are they?

A

= dome shape

= purple
meaning lots of nuclei

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12
Q

how do M cells take up antigens?

A

= by endocytosis and phagocytosis

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13
Q

how are antigens transported across the M cells and where are they released?

A 
Transported = in vesicles and 
Released = at basal surface
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14
Q

what is the antigen bound by?

A

= dendritic cells, activating T cells

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15
Q

Yes or No.

can dendritic cells extend processes across the epithelial layer?

A

Yes.

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16
Q

why do dendritic cells extend processes across the epithelial layer?

A

= two capture antigen from lumen of the gut

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17
Q

what 2 components does the mucosal of the immune system consist of?

A

1) epithelium

2) lamina propria

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18
Q

what type of immune cells are contained in the epithelia?

A

intra-epithelial lymphocytes

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19
Q

how do T cells enter Peyer’s patches?

A

from blood vessels, directed by the homing receptor CCR7 and L-selectin

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20
Q

what do these T cells in the Peyer’s patch then encounter?

A

= encounter antigens transported across M cells and become activated by dendritic cells.

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21
Q

what do the activated T cells then?

A

= drain via mesenteric Lymph nodes to thoracic duct and returns to gut via bloodstream

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22
Q

what do acivated T cells express?

A

alpha 4; beta 7 integral
and
CCR9 ome ot lamina propria and intestinale epithelium of small intestine

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23
Q

what do gut-homing effector T cells bind?

A

= bind MAdCAM-1 on endothelium

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24
Q

what do gut epithelial cells express?

A

chemokine specific for gut-homing T cells

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25
Q

where else is MAdCAM also found?

A

= in vasculature of other mucosal sites.

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26
Q

what can lymphocytes primed in the guts do?

A

= migrate to other mucosal sites

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27
Q

how do passive immunity transfer?

A

in breast milk

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28
Q

what are 3 humeral intestinal responses?

A

IgA = 80%
= dimeric
IgM = 15%
IgG = 5%

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29
Q

Yes or No.

Reversal of systemic humeral immune response; IgG, IgM, IgA monomeric?

A

Yes

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30
Q

where does IgA bind?

A

= to receptor on basolateral face of epithelial cells

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31
Q

what does IgA binding to receptor on baso-lateral face of epithelial cells cause?

A

= endocytosis

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32
Q

what happens after endocytosis?

A

= transcytosis to apical face of epithelial cells

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33
Q

after transcytosis to apical face of epithelial cells, what happens?

A

= release of IgA dimer at apical face of epithelial cells

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34
Q

what can secreted IgA on the gut surface do?

A

= bind and neutralise pathhogens and toxins

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35
Q

what is IgA also able to bind and neutralise?

A

antigens internalised in endoscomes

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36
Q

what can IgA export?

A

toxins and pathogens from lamina propria while being secreted

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37
Q

what does the activated appearance on special T cells contain?

A

full killing machinery

38
Q

describe the antigen receptor repertoire on special T cells?

A

= restricted antigen receptor repertoire

39
Q

describe the different recognition mechanisms.

A

2 types with different recognition mechanisms

40
Q

describe the different recognition mechanisms.

A

2 types with different recognition mechanisms

41
Q

what type of lymphocytes lie within epithelial lining of gut?

A

= intra-epithelial lymphocytes (IELS)

42
Q

what are intra-epithelial lymphocytes positive?

A

CD8-positive T cells

43
Q

at higher magnification, what can the ILEs be seen to lie within?

A

the epithelial layer between epithelial cells

44
Q

what happens after the virus has infected mucosal epithelium cells?

A

infected cells display viral peptide to CD8 IEL via MHC class I

45
Q

what do activated IEL kill?

A

infected epithelial cells by perform/granzyme and Fas dependent pathway

46
Q

what do epithelial cells undergo as a result of infection, damage or toxic peptide?

A

= stress and express MIC-A and MIC-B

47
Q

what binds to MIC-A,B and as a result activated IEL?

A

NKG2D on IELs bind

48
Q

what else binds o TL?

A

CD8Alpha:alpha homodimers

49
Q

what do activated IELs kill?

A

the stressed cell via perforin/granzyme pathway

50
Q

what needs to happen to maintain the balance between protective immunity and homeostasis?

A

= discriminating between pathogen and innocuous antigens

51
Q

what happens after oral administration of protein state of specific peripheral unresponsiveness = oral tolerance?

A

= default response

52
Q

What is inhibited more - T cell &IgE mediated responses or serum IgG responses?

A

T cells and IgE mediated responses are inhibited more than serum IgG responses both locally and systemically

53
Q

proposed mechanism

A

proposed mechanism

54
Q

proposed mechanism

A

proposed mechanism

55
Q

proposed mechanism

A

proposed mechanism

56
Q

proposed mechanism

A

proposed mechaism

57
Q

how does pathogen recognition occur by and what does this initiate?

A

= TLRs, initiating a cascade of signals that activate IKK

58
Q

what does IKK phosphorylate?

A

= IKB, targeting it to be degraded

- NFKB translocates to the nucleus to activate gene transcription

59
Q

what blocks gene transcription, by activated PRARgamma, which removes NFKB from nucleus?

A

some commensal bacterial

60
Q

what can some commensal bacteria block?

A

degradation of phosphorylated IKBs, preventing NFKB trans-location to the nucleus

61
Q

look at slide 29

A

look at slide 29

62
Q

what are 5 roles of intestinal mucosal in imm unity in disease?

A
  • infectious disease
  • primary immunodeficiency
  • allergy
  • coeliac disease
  • IBD
63
Q

what type of immune mechanism eliminates most intestinal infections rapidly?

A

= innate mechanisms

64
Q

how does the immune mechanism work?

A

= activation though ligation of pattern recognition receptors
= intracellular sensors in epithelial cells, PRR, activate NFkB pathway
= gene transcription and production of cytokines, chemokines an defensives
= activation of underlying immune response

65
Q

what is the outcome of infection by intestinal pathogens determined by?

A

= complex interplay between micro-organism and host

66
Q

See slide 32 on diagram.

A

See slide 32 on diagram

67
Q

what do infected dendritic cells shuttle?

A

= shuttle virus from site of exposure to regional lymph nodes where they concentrate virus particle and infect CD4+ T cells

68
Q

what are 5 mucosal disorders associated with primary immuno-deficiency?

A

1) Selective IgA deficiency -2/3 asymptomatic remainder recurrent sinopulmonary infections (Coeliac disease 10x)

2) CVID - recurrent sinopulmonary and GI infections
= failure to differentiate into Ig secreting cells
= Low IgG, IgA, IgM and IgE
= Defective antigen specific antibody response

3) XLA - Sinopulmonary and GI infections+ devastating systemic manifestations of chronic enteroviral infections
No B cells/ agammaglobulinaemia

4) CGD - Staphlococcus aureus/inflammatory granulomas- pneumona, liver abscess, perianal abscess and skin abscess.
Failure of phagocyte respiratory burst

5) SCID- Profound defect in T and B cell immunity
oral candidiasis/chronic diarrhoea/interstitial pneumonitis
GI- CMV/rotavirus/EBV

69
Q

what type of hypersensitivity is associated by food allergy?

A

= type I hypersensitivity reaction

70
Q

how is type I hyper-sensitivity reaction initiated by?

A

= cross linking allergen specific IgE on surface of mast cells with the specific allergen
= memory response-immune system must be primed

71
Q

what does IgE secreted by plasma cells bind to?

A

a high-affinity Fc receptor FcgammeRI on mast cell

72
Q

what do activated mast cells provide?

A

= contact and secreted signals to B cells to stimulate IgE production

73
Q

see IgE mediated allergic reactions slide 37

A

see IgE mediated allergic reactions slide 37

74
Q

see slide 38

A

see slide 38

75
Q

what is coeliac disease/gluten sensitive enteropathy?

A

= genetically linked, (auto) immune disorder, causing damage to small intestine leading to malnutrition

  • life long, incurable
  • NOT an allergy
76
Q

what genes make you susceptible to coeliac disease?

A

HLADQ2

HLADQ8

77
Q

describe gamma interferon in coeliac disease?

A

Gamma interferon from Gluten specific T cell activate epithelial cells which produce IL-15 which induces proliferation and activation of IEL
- Both T cells and IEL can then kill epithelial cells

78
Q

see slide 41 on diagrams

A

see slide 41 on diagram

79
Q

describe transamination of gliadin peptide and activation of gliadin-specific T cell.

A

leads to activation of plasma cells and other lymphocytes.

- cytokines released by activated lymphocytes lead to damage to intestinal epithelium

80
Q

look at slide 44 diagrams.

A

look at slide 44 diagram

81
Q

how do you diagnose coeliac disease?

A

= biopsy

= serology, useful as screening test IgA anti-tissue trans-glutaminase auto-antibodies

82
Q

what is Crohn’s disease

A

= can affect any part of the GI tract from mouth to anus - commonly distal ileum and colon

= focal and discontinuous inflammation with deep and eroding fissures +/- granulomas

83
Q

how is Crohn’s disease mediated by?

A

= Th1 CD4+ T cells/gamma interferon/IL-12/TNF alpha

84
Q

Yes or No.

Is it a multiple genetic deficiency and immunological mechanism - multi-factorial - HLA.

A

Yes.

85
Q

what gene is identified in Crohn’s disease?

A

= NOD2

- intracellular PRR muramyl dipeptide of bacterial peptidoglycan

86
Q

describe the interleukins identified in Crohn’s disease?

A

IL-8 and neutrophil function
AND
IL-23/atuophagy

87
Q

what is ulcerative colitis restrictive to?

A

= retracted to rectum and colon

  • starts in rectum and moves proximally and contiguously (and develops extra-intestinal manifestations)
  • inflammation and ulceration just in surface mucosa
88
Q

what infiltrates the distortion of crypts?

A

= infiltration of monocytes/neutrophills and plasma cells

89
Q

Yes or No.

Does immuno-pathology fit into Th1/Th2?

A

= no

- postulated may be an NK T cell mediated disease via IL-13

90
Q

what do both conditions produce large amounts of?

A

= large amounts of inflammatory cytokines IL-1, IL-6 and TNF alpha

91
Q

how would you treat these conditions?

A

= non-specific anti-inflammatory and immune-suppressive drugs steroids, azathioprine, cyclosporin, methotrexate
= anti-TNF alpha

GI (43 decks)

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