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1. GI > Mucosal Immunity > Flashcards

Mucosal Immunity Flashcards

1
Q

What is the function of mucosal surfaces?

A
  • Gas exchange
  • Food adsorption
  • Sensory activities
  • Reproduction
  • Portal of entry for non pathogenic antigens
    (main site of infection)
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2
Q

How does an immune response occur in a lymph node?

A

Dendritic cells enter the paracortical area and look for T cells.
If there is the correct match of dendritic cells, T cells and antigens then an immune response occurs

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3
Q

What occurs at specialised lymphoid tissue?

A

site of antigen sampling in the gut

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4
Q

Where do effector mechanisms happen?

A

lamina propria

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5
Q

What is a Peyer Patch?

A
  • covered by an epithelial layer which contains specialised M cells (covered in microvilli)
  • dentritic cells in the peyers patch sample antigens from the M cells
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6
Q

How are T cells activated in the gut?

A

M cells take up antigens by phagocytosis and endocytosis
Antigens are transpored across the M cells in vesicles and released at the basal surface
Antigen is bound to dentritic cells, which activates T cells

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7
Q

What are other the ways (apart from from the epithelium) that dendritic cells can sample antigens?

A

lamina propria

- can extend processes through the epithelium and capture antigens from the lumen of the gut

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8
Q

What are the immune cells of the lamina propria?

A 
CD4 T cell
Dendritic cell 
Macrophage
Mast cell
Plasma cell
IgA
a4B7 integrin
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9
Q

What are the immune cells of the epithelium?

A

a4B7 integrin
Dendritic cell
CD8 T cell

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10
Q

In what form is IgA in the gut?

A

Monomeric

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11
Q

How are T cells contained in the gut?

A
  • T cells enter peyers patches from blood vessels (directed by homing receptors CCR7 and L selectin)
  • T cells in the Peyers patch encounter antigen transported across M cells and become activated by dendritic cells
  • Activated T cells drain via mesenteric lymph nodes to the thoracic duct and return to the gut via the bloodstream
  • Activated T cells expressing a4:B7 integrin and CCR9 home to the lamina propriety and intestinal epithelium of the small intestine
  • Gut homing effector T cells bind MAdCAM-1 on endothelium
  • Gut epithelial cells express chemokines specidfic for gut-homing T cells
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12
Q

How is IgA re?leased from an epithelial cell

A
  • IgA binds to receptor on basolateral face of epithelial cell
  • endocytosis occurs
  • transcytosis to apical face of epithelial cell
  • release of IgA dimer
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13
Q

Which part of IgA needs protected?

A

hinge region

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14
Q

What can replace IgA if someone has an IgA deficiency?

A

IgM

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15
Q

What does IgA prevent?

A

damage from epithelial cells

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16
Q

What are intraepithelial lymphocytes?

What are they responsible for?

A

–90% T cells with 80% CD8+
–Activated appearance containing full killing machinery
–Restricted antigen receptor repertoire
–Expression of aE:b7 integrin - anchors them in the epithelium
–2 types with different recognition mechanisms

Major cause of the immunopathology of coeliac disease

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17
Q

Where do intraepithelial cells lie?

A

within the epithelial gut lining

18
Q

What happens when a virus infects a mucosal epithelium cell?

A
  • infected cell displays viral peptide to CD8 IEL via MHC class 1
  • activated IEL kills infected epithelial cell by perforin/granzyme and Fas-dependant pathway
19
Q

What are the features of activated IELs?

A

Detect the infection and they directly kill only the cell that is infected – do it for virus and stress
Protects the cells around it

20
Q

What occurs when there are lots of killed epithelium cells?

A

flattened epithelium

i.e. coeliac disease

21
Q

What does mucosal hyperresponsiveness cause?

A

Crohn’s disease

22
Q

What is the mechanisms of mucosal hyperresponsiveness?

A
  • Responses needing controlled in the gut: T cells and IgE (as they cause damage)
  • Commensal organisms help regulate local hyporesponsiveness- PPAR gamma
  • Anergy or deletion of antigen specific T cells- no costimulation
  • Generation of regulatory T cells particularly CD4+ TGF b producing Th3 cells- weak costimulation: Both Immunosuppressive and induces switching of B cells to IgA production
23
Q

What is the normal dendritic cell response to commensal bacteria?

A
  • production of PGE2, TGF-B and TSLP which inhibits dendritic cell maturation
  • immature dendritic cells give weak co-stimulatory signals and induce CD4 T cells to differentiate into regulatory Th3 or Treg cells
24
Q

What is the dendritic cell repsonse to invasive microorganisms?

A
  • invasive microorganisms penetrate epithelium to activate dendritic cells
  • activated dendritic cells express strong co-stimulatory ligands and induce CD4 T cells to differentiate into effector Th1 and Th2 cells
25
Q

What is the mucosal response to infection?

A
  • Innate mechanisms eliminate most intestinal infections rapidly
  • Activation through ligation of pattern recognition receptors
  • Intracellular sensors in epithelial cells, PRR, activate the NFkB pathway
  • Gene transcription and production of cytokines, chemokines and defensins
  • Activation of underlying immune response
26
Q

How are inflammatory cytokines, chemokines and other mediators expressed on the epithelial cell?

A

TLRs, NDO1 and NDO2 activate NFkB which induces the epithelial cell to express them

27
Q

What is the role of Th2 in the gut?

A
  • protective = releases lots of cytokines
  • releases IL3 (induces epithelial cell repair) and IL5 (recruits and activates eosinophils)
  • produces IgE (through B cells)
28
Q

What is the role of Th1 in the gut?

A
  • host damage

- activate macrophages and B cells (to produce IgG2a)

29
Q

What happens when the mucosal immunity becomes deregulated?

A

Infected dendritic cells shuttle virus from the site of exposure to the regional lymph nodes where they concentrate virus particles and infect CD4+ T cells

30
Q

What is SCID?

A

defect in T and B cell immunity - presents earlier in life than others as there is no IgG to protect them

31
Q

What is Selective IgA deficiency?

A

asymptomatic remainder recurrent sinopulmonary infections

32
Q

What is CVID?

A

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

33
Q

What is XLA?

A

Sinopulmonary and GI infections + devastating systemic manifestations of chronic enteroviral infections (xlinked so boys)
–No B cells/ agammaglobulinaemia

34
Q

What is CGD?

A

children that present with: Staphlococcus aureus/inflammatory granulomas

  • mostly boys
  • failure of phagocyte respiratory burst
35
Q

What is a food allergy?

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

36
Q

What is Coeliac disease mediated by?

A

T cells

37
Q

Describe the immunology of Coeliac disease?

A

T cell/IEL mediated
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

38
Q

How is Coeliac disease diagnosed?

A

biopsy - not for children though

39
Q

Describe Crohn’s disease?

A

Focal and discontinous inflammation with deep and eroding fissures +/- granulomas
Mediated by Th1 CD4+ T cells/gamma interferon/IL-12/ TNF alpha
Multiple genetic deficiency and immunologic mechanisms- multifactorial- HLA
Gene identified NOD2 (10-15%)- intracellular PRR- muramyl dipeptide of bacterial peptidoglycan

40
Q

What is the most common social background to develop ulcerative colitis?

A

children of immigrants

41
Q

Describe Ulcerative Colitis?

A

Produces large amounts of inflammatory cytokines IL-1, IL-6 and TNF alpha
Restricted to rectum and colon

1. GI (61 decks)

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