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GI > Mucosal Immunity > Flashcards

Mucosal Immunity Flashcards

1
Q

what are the physiological functions of mucosal tissues

A

gas exchange, food absorption, sensory activities, reproduction

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2
Q

what makes the mucosal tissues highly vulnerable

A

fragile and permeable

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3
Q

give an example of a non pathogenic antigen

A

dietary protein

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4
Q

what does trans and para cellular mean

A

para- travelling in tight gap between

trans- travelling through cells

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5
Q

describe how the mucosal tissues of the body are unified

A

an immune response in one can be common in all sites

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6
Q

what are the mucosal tissues of the body

A

GI tract, resp tract, uro-genital tract, mammary glands, kidney

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7
Q

what is the role of the primary lymphoid tissue

A

regulate and monitor antigen passage

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8
Q

how do immune cells evoke a response in the lymph nodes

A

dendritic cells come to the lymph nodes with antigens and look for T cells that will recognise antigens- if found = immune response, proliferation, differentiation and production of antibodies

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9
Q

describe the anatomical features (3) of the gut mucosal immune system

A

intimate relationship between mucosal epthelia and lymphoid tissue

organised lymphoid tissue structures unique to mucosal sites

specialised antigen uptake mechanisms to maximise sampling

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10
Q

what are the effector mechanisms of the gut mucosal immune system

A

activates/ memory T cells

natural effector/ regulatory T cells responsible for down regulating immune response aswell

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11
Q

what are effectors and roles of the immmunoregulatory environment within the gut mucosal immune system

A

inhibitory macrophages and tolerising dendritic cells

active down regulation of immune response

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12
Q

what is peyers patch

A

specialised lymph node (secondary lymph tissue) that sits in the epithelium of the gut, site of antigen sampling of gut contents

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13
Q

where are lymphoid tissues found in the gut

A

scattered throughout lamina propria of intestine and in organised lymphoid tissues- peyers patch

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14
Q

what covers the peyers patch

A

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

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15
Q

describe the structure and role of M cells

A

M for microvilli which cover the surface to increase SA

antigen sampling- acts as a gateway to peyers patch. beneath M cell in dendritic cell that processes and presents antigen to T cells which leave patch and move to mesentery lymph nodes

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16
Q

how do M cells sample the gut contents and transport the antigens to the T cells

A

M cells take up antigen by endocytosis and phagocytosis

antigen is transported across the M cell in vesicles and released at the basal surface

antigen is bound by dendritic cells which activate T cells

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17
Q

how can dendritic cells sample the gut contents

A

can extend processes across the epithelial layer

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18
Q

what is the main site of antigen sampling

A

lamina propria

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19
Q

what are to distinct compartments of the mucosal immune system

A

the epithelium and the lamina propria

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20
Q

what are the immune cells of the lamina propria

A

CD4 T cells, dendritic, macrophage, mast, DC, IgA, plasma cell

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21
Q

what are the immune cells of the epithelial layer

A

CD8 T cells, dendritic cells

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22
Q

describe the pathway of T cells to and from the peyers patch

A

enter via bloodstream, activated, drain via mesenteric lymph nodes to the thoracic duct, return to gut via blood stream, travel to lamina propria to carry out effector function

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23
Q

how does the T cell leave the small intestine

A

gut homing effector T cells bind to MAdCAM-1 on endothelium

gut epithelial cells express chemokines specific for gut homing T cells which allow the movement into the lamina propria

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24
Q

where can lymphocytes primed in the gut migrate to

A

other mucosal sites

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25
Q

what is the most common imunoglobulin in the intestine

A

IgA (mucosa) 80%
IgM 15%
IgG 5 %

reverse of systemic immune response

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26
Q

what does a dimeric immunoglobulin mean

A

two molecules joined together by a J (joining) chain

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27
Q

what path do immunoglobins take in the intestine immune response

A

binds to receptor on basolateral face of epithelial cell ( in lamina propria)

endocytosis and transcytosis to the apical face of cell

released into lumen

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28
Q

what is the role of the IgA that is released into the lumen

A

bind to and neutralise pathogens and toxins

is then internalised by endosomes

exports toxins and pathogens form the lamina propria

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29
Q

how can people with IgA deficiency be a-symptomatic

A

as IgM can replace IgA as is also a polymeric Ig can used same polymeric Ig receptor on epithelial cells

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30
Q

what is the most common intraepithelial lymphoctye

A

90% T cells (80% of these T cells CD8+)

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31
Q

why dont intraepithelial lymphocytes have normal function

A

as they have resticited antigen receptor repertoire and are anchored to the epithelial lining by an intergrin

32
Q

what is the role of intraepithelial lymphoctyes

A

virus infects mucosal epithelium cell

infected cell displays viral peptide to CD8 IEL via MHC class I

activated IEL kills infected epithelial cell by perforin/granzyme and Fas-dependent pathways

33
Q

when do epithelial cells undergo stress

A

as a result of an infection, damage, toxic peptides

34
Q

what happens to stressed epithelial cells

A

stress receptors

killed by activated IEL via the perforin/granzyme pathway

protect cells around stressed one

35
Q

what happens to the epithelium when cells start to get killed

A

flattened epithelium as cells cannot be produced from the crypts as fast as they are being killed

36
Q

what is oral tolerance

A

Default response to oral administration of protein state of specific peripheral unresponsiveness

body has discriminated between pathogen and innocuous agent

37
Q

what immune responses are mediated the most and why

A

T cell and IgE responses as these are the ones that cause damage do the host

38
Q

what do commensal organism help with

A

regulate local hyporesponsiveness

39
Q

what are the mechanisms of mucosal hyporesponsiveness

A

Anergy or deletion of antigen specific T cells- no costimulation

(anery = absence of the normal immune response to a particular antigen or allergen)

Generation of regulatory T cells- weak costimulation

both induce B cells to make IgA which is protective not inflammatory

40
Q

what causes crohns disease

A

inappropriate responses to commensal organisms

41
Q

how do commensal bacteria regulate hyporesponsiveness

A

block gene transcription and inhibit dendritic cell maturation leading to CD4 T cells differentiating into TH3 or Treg cells

42
Q

how do pathogens not cause hyporesponsiveness

A

active gene transcription and activate dendritic cells meaning CD4 T cells differentiate into TH1 and TH2 cells

43
Q

what is the mucosal response to infection

A

innate mechanisms eliminate most intestinal infections rapidly

activation through ligation of pattern recognition receptors (e.g. on dendritic cells)

intracellular sensors in epithelial cells (PRR) activate the NFkB

Gene transcription and production of cytokines, chemokines and defensins

activation of underlying immune response

44
Q

what is the outcome of intestinal pathogens determined by

A

the microorganism and the host immune response:

CD4 T cells activated and can differentiate into TH1 (host damage) or TH2 cells (protective)

45
Q

what are the effector functions of TH2

A

TH2 usually protective, induces cytokines:
-(IL 13) increases the production of mucous and induces epithelial cell repair
-(IL 5) recruits and activate eosinophils
-(IL 3 and 9) drive mast cell recruitment
drive B cells to produce IgE

46
Q

what are TH1 cell effector functions

A

activate macrophages

activate B cells to produce IgG2a

47
Q

what is the main antibody for parasites

A

IgE

48
Q

how does the HIV virus dysregulate mucosal immunity

A

destroys memory cells:
HIV infects dendritic cells, uses dendritic cell activation to move itself to lymph nodes where it infected T cells, activating them, using them to move back to mucosal sites and infect all CD4 cells in mucosal site, enters blood stream and causes widespread dissemination

49
Q

what is the most common mucosal disorder associates with primary immuno deficiency

A

selective IgA deficiency

50
Q

what is CVID and describe it

A

common variable immune deficiency

  • recurrent sinopulmonary and GI bacterial infections, presents in adulthood
  • failure to differentiate Ig secreting cells do low immunoglobulins
  • can cause irrversible damage e.g bronchiectasis
51
Q

what is XLA, describe it

A

x linked agammaglobulinaemia

  • sinopulmonary and GI infection
  • no B cells
  • presents in boys at 7-8 months as IgA from breast milk stopped
52
Q

what is CGD, describe it

A

chronic granulomatuos disease

  • staphylococcus aureus/inflammatory granulomas infections (pneumonia, liver abscess, liver perianal and skin abscess)
  • failure of phagocyte respiratory burst (how neutrophils kill pathogens)
53
Q

what is SCID, define it

A

severe combined immunodeficiency

  • T and B cell defects
  • present in early life with fungal and viral infections
54
Q

what is a food allergy reaction caused by

A

Type I hypersensitivity reaction initiated by crosslinking of allergen specific IgE on the surface of mast cells with the specific allergen.
Memory response- immune system must be primed

55
Q

why do food allergens affect the body in a similar way to venoms or IV drugs

A

as venoms and drugs in bloodstream, cause a response in epithelium mast cells

food passes as unprocessed proteins through into bloodstream from gut

56
Q

how are mast cells involved in an allergic reaction

A

IgE binds to FC receptor on mast cells activating them. Activated mast cells provide contact and secreted signals to B cells to stimulate IgE production
cause
-release of histamine
-cause rhinitis and asthma due to contraction of bronchial smooth muscle and increased mucous secretion
-causes contraction of intestinal smooth muscle causes vomiting

57
Q

what is coeliac disease

A

gluten sensitivity enteropathy- genetically linked auto-immune disorder causing damage to the small intestine leading to malnutrition

58
Q

how is coeliac cured/ treated

A

incurable, treated via avoidance of gluten

59
Q

is coeliac disease an allergy

A

no- as not mediated by IgE, instead mediated by T cells and IEL

60
Q

what is thought to cause coeliac

A

genetic susceptibility, trigger unknown

61
Q

what is the immune pathway of 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

62
Q

what component of the immune system leads to the damage of the intestinal epithelium

A

cytokines released by activated lymphocytes

63
Q

what happens when a coeliac stops eating gluten

A

the damaged, lymphocyte infiltrated enterocytes are replaced by normal columnar ones, assuring normal transport from the body into the lumen, gut returns to normal

64
Q

how is coeliac disease diagnosed

A

biopsy, serology for IgA anti- TTG

65
Q

what is anti tTG antibody

A

produced by B cells, helped by T cells, in response to gluten tTg complex (in coeliac disease)

66
Q

what part of the GI tract does crohns afffect

A

any part- from mouth to anus- commonly distal ileum and colon

67
Q

what is crohns disease characterised by

A

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

68
Q

what mediates crohns disease

A

TH1, CD4+ T cells, gamma interferon, IL-12, TNF alpha (really inflammatory) - T cell mediated

69
Q

what is thought to cause crohns disease

A

multiple genetic deficiency and immunologic mechanisms (multifactoral)

70
Q

what is crohns a form of

A

inflammatory bowl disease

71
Q

what is ulcerative colitis

A

form of inflammatory bowl disease

72
Q

what part of GI tract is affected by UC

A

restricted to rectum and colon- starts in colon and moves proximally and contiguously (can develop extra intestinal manifestations- arthritis, uveitis and skin lesions)

73
Q

what is UC characterised by

A

distortion of the crypts with infiltration of monocytes/ neutrophils and plasma cells
inflammation and ulceration in the surface mucosa

74
Q

what cant you make without IgA

A

antibodies

75
Q

in both crohns and UC what is produced in large amount

A

the inflammatory cytokines IL-1, IL-6 and TNF alpha

76
Q

what are the pharmacological treatements for crohns and UC

A

Non specific anti-inflammatory and immunosuppressive drugs steroids/azathioprine/cyclosporin/methotrexate

anti-TNF alpha

GI (64 decks)

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