Mucosal Immunity Flashcards

1
Q

Where are the mucosa found ?

A

Lungs, gut, eyes, nose, uterus etc

  • Where most infection enters - needs to be semi-permeable as is constantly interacting with pathogens
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2
Q

How does the mucosa’s immune response work?

A
  • Is a balance between an overt immune response and a tolerogenic response
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3
Q

What Is a MALT and give an example (2 points)

A
  • Mucosa associated lymphoid tissue
  • e.g., Peyers patches in gut - have high population of B-cells - interact with DCs - migrate to lymph node
  • Then home back to where the infection was found - specific antigen
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4
Q

What allows the mucosa to respond very quickly to infection?

A

Because they do not need to be primed by Dendritic cells first

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5
Q

What does the mucosa use as its effectors?

A

IgA antibodies

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6
Q

Why will the mucosa not usually trigger an overt response? 1 point

A

Mucosal tissue contains a high abundance of tolerogenic cytokines e.g., TGF-beta

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7
Q

For each structure in the gut, what does stem cell differentiation create?

A

enterocytes - absorptive - AMPs production
Paneth cells - antimicrobial peptide production - AMPs
Goblet cells - mucus secretion

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8
Q

How is IgA excluded?

A

plgR - binds to IgA - and it is exocytosed into the gut lumen

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9
Q

What are IELs and what are the two types?

A

Intraepithelial Lymphocytes

Type 1: Similar to CD8 cells but are already primed - and have an activated phenotype

  • can rapidly recognise abnormal phenotypes expressed by cells and eliminate epithelial cells in presence of infection

Type 2: Activated IELS- but don’t interact with MHC peptide complexes

  • Interact with MHC like molecules on stress cells
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10
Q

How is celiacs disease caused?

A

Caused by overt/excessive activation of IELs

  • HLA-DQ2 - binds gliadin - lymphocyte mediated
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11
Q

What are ILCs?

A

Innate lymphoid cells - counterpart of CD4+ T helper cells

  • Secrete cytokines that respond quickly to pathogenic tissue damage
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12
Q

What are ILCs equivalents to in helper cells?

A

Group 1 ILCs - Th1 cells

Group 2 ILCs - Th2 - secrete IL-4/5/9/13 - activate eosinophils + wound repair - skew B cell development

Group 3 ILCs - Th17/Th22 - defensives - mucus - antic peptides - are ready to secrete cytokines and skew/enhance immune response

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13
Q

Function of DCs

A
  • Constantly sampling antigens from environment and presenting them to T cells
  • Trigger T cells - CD4+ and CD8 cytotoxic
  • T and B cell maturation
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14
Q

How are tolerogenic DCs different?

A
  • Secrete anti-inflammatory - T regs - CD103+

- Imprint homing and upregulate - so T and B cells just continue circulating and are not matured

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15
Q

How does the mucosa interact with commensal bacteria?

A
  • Interact in happy equilibrium
  • Extract and synthesise metabolites
  • They compete with unwanted pathogens - inhibit pathway required for pathogen uptake
  • Small reactions - tolerogenic - low level inflammatory response - don’t want big response as it would kill them all
  • Commensals actively down regulate the inflammatory pathway
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16
Q

What is down regulated in the gut during a response to mucosal pathogens? What is there instead?

A

Toll like receptors - not expressed on apical surface

Have intracellular pattern recognition receptors

17
Q

What occurs when cells have been invaded by pathogens in the mucosa?

A

Recognised by N0D1/N0D2 and NFkB signalling is initiated

  • Which switches on pro-inflammatory cytokines
  • Recognition by PRRs triggers innate response - DC activation - adaptive immunity
18
Q

Where are pattern recognition receptors found in the mucosa?

A

Basal surface - not on the surface of cell as normal

19
Q

How does salmonella evade the immune system

A

Escapes vacuoles and hides in cytosol

  • Escapes cell surface PRRs
20
Q

Name 2 pro-inflammatory cytokines

A

IL-1, IL-18

21
Q

Name 2 anti-inflammatory cytokines

A

IL-10, TGF-beta

22
Q

How does Shigella work?

A

Invades via mucosal cells - and kills cells

  • Has a toxin that inhibits translation
  • C.difficile - toxin A - inactivates GTPases
23
Q

What do Helminths infections provoke?

A

Strong Type-2 responses

  • Production of non-phagocytic cells - helps eliminate some of the larger infections
24
Q

How is Crohns disease caused?

A

Over-activation of intracellular PRR N0D2, Atg16L1

  • Autophagy - causes sustained microbial induced inflammation - innate mediated