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Gastrointestinal pathophysiology > Immunology of the gut > Flashcards

Immunology of the gut Flashcards

1
Q

Why do the majority of infectious agents invade the human body via mucosal surfaces?

A

Because their physiological function in gas exchange (lungs), food adsorption (gut), sensory activities (nose, mouth), mucosal surfaces are thin and permeable barriers to the interior of the body.

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2
Q

The cells of the mucosal immune system are found where?

A

Within the lamina propria

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3
Q

The lamina propria is separated from the lumen by …

A

A single layer of epithelium

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4
Q

The most common epithelial cells of the intestinal epithelium are?

A
  1. Enterocytes/colonocytes
  2. Goblet cells
  3. Paneth cells
  4. Tuft cells
  5. Enteroendocrine cells
  6. M cells
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5
Q

Enterocytes/colonocytes are connected by proteins called what?

A

Tight junctions, e.g. occludins and claudins

- These make the epithelial cells stick tightly together so nothing can get to the lamina propria

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6
Q

Role of paneth cells?

A

Secrete antimicrobial peptides

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7
Q

Role of goblet cells?

A

Produce mucins which form a mucus layer making it harder for microbes to come into contact with epithelial cells

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8
Q

MALT can be divided into what?

A

NALT - lining of nose
BALT - URT
GALT

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9
Q

The innate immune response is carried out by which cells?

A
  1. Dendritic cells
  2. Macrophages
  3. Monocytes
  4. Granulocytes (neutrophils, eosinophils, basophils)
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10
Q

The adaptive immune response is carried out by which cells?

A
  1. CD4+ T helper cells
  2. CD8+ T cytotoxic cells
  3. B cells
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11
Q

Innate vs adaptive recognition of antigen?

A

Innate: Pattern recognition receptors e.g toll-like receptors/NODs/CARDs
- Recognise patterns/motifs e.g. peptidoglycan, LPS, dsRNA

Adaptive: T-cell receptor (TCR) and B-cell receptor (BCR)

  • Recognise specific Ag
  • T cells = recognise peptide/MHC complex
  • B cells = recognise 3D structure
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12
Q

CD4+ T helper cells come as effector subsets and regulatory subsets, what are examples of each?

A
  1. Effector subsets = help us fight pathogens
    - Th1 = IFN-gamma
    - Th2 = IL4, IL5
    - Th17 - IL17
  2. Regulatory subsets = regulate/dampen the effectors
    - Tr1 = IL10
    - Th3 = TGF-beta
    - CD25+ = IL10 and TGF-beta
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13
Q

The Th1, Th2 and Th17 effector subsets are involved in which pathologies?

A
  1. Th1 - IFN-gamma - chronic inflammation & autoimmunity (type 1 diabetes?)
  2. Th2 - IL4/IL5 - Allergy asthma
  3. Th17 - IL17 - Chronic inflammation, autoimmunity (RA, MS, psoriasis, IBD?)
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14
Q

GALT is divided into organised tissues and scattered lymphoid tissues, what are examples of each?

A
  1. Organised tissues
    - Peyer’s patches (in SI)
    - Isolated lymphoid follicles (in SI and LI)
    - Mesenteric lymph nodes
  2. Scattered lymphoid cells
    - Lamina propria leukocytes
    - Intraepithelial lymphocytes
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15
Q

What is the largest lymph node in the body?

A

Mesenteric lymph nodes - they drain the intestinal tract

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16
Q

Where are peyer’s patches found?

A

Just beneath the epithelial layer

17
Q

Lamina propria leukocytes (LPL) are found where?

A

In the lamina propria

18
Q

Intraepithelial leukocytes (IEL) are found where?

A

In the epithelial layer, for every 10 epithelial cells you have 1 IEL

19
Q

What are IELs?

A

Specialised types of T cells mainly found in the gut

20
Q

What other cells are found within the lamina propria with the LPLs?

A

Mucosal immune system cells

  • CD4+
  • CD8+
  • Dendritic cells
  • Plasma cells
  • Macrophages
21
Q

Why are immune system responses generated in the GALT distinct from those after immunisation or when an antigen enters the blood stream?

A

Because the GALT has its own contents of lymphoid cells, hormone, and other immunomodulatory factors

22
Q

Antigens present at the mucosal surfaces must be transported across an epithelial barrier before they can stimulate the mucosal immune system, how is this done?

A
  1. Mechanism 1: M cells sit on top of Peyer’s patches are also found on top of isolated lymphoid follicles, they are involved in the taking up of and transporting of antigens to new cells in the lamina propria
  2. Mechanism 2: They are taken up by macrophages which are extending processes in between epithelial cells which extend processes across the epithelial layer to capture antigens from the lumen of the gut
    - Macrophages are not good at migrating so they hand over the Ag to DCs in the lamina propria, these Ag-loaded DCs migrate via drainage lymphatics to the mesenteric lymph nodes where they activate T cells
23
Q

Which pathogens target M cells to gain access to the subepithelial space, into the body?

A
  • Poliovirus
  • Reovirus
  • Some retroviruses: salmonella, shigella and yersinia
24
Q

How do M cells transport antigens to the lamina propria?

A
  1. M cell takes up the antigen by endocytosis and phagocytosis
  2. Antigen is transported across the M cell down towards the basolateral site of the epithelium, here you will have cells of the immune system such as DCs
  3. The antigen is bound by DCs, which migrate to T cell areas within the Peyer’s patch and they can also migrate via drainage lymphatics to the mesenteric lymph nodes, where they activate T cells
25
Q

Give the different ways in which macrophages and dendritic cells are conditioned within our healthy intestines are conditioned

A
  • In the lamina propria there are factors which make them anti-inflammatory:
    1. Epithelial cells sense components of commensal bacteria and in turn release TSLP from epithelial cells which act on DCs
  1. Vit A release retinoic acid which act on DCs
  2. TGF-beta acts on macrophages and DCs
  3. Bacterial products condition DCs, such as short chain fatty acids e.g. butyrate, acetate and proprionate. These are metabolites of bacteria
26
Q

In the healthy intestine, what do macrophages secrete?

A

Anti-inflammatory IL10

27
Q

In the healthy intestine, what do DCs secrete?

A

TGF-beta

28
Q

Due to the conditioning, which specific cell response do DCs favour?

A

Treg cell response (once they have migrated to mesenteric LNs with the Ag

29
Q

Explain how intestinal homeostasis is maintained and how we end up with inflammation

A
  1. Intestinal homeostasis is maintained by a balance between effector T cells and regulatory T cells
  2. Either too many effectors, so Tregs cant handle them, cause inflammation of the intestine OR a Treg defect so they cant balance the effector cells, causing an imbalance, leading to intestinal inflammation
30
Q

What is the dominant antibody class in the mucosal immune system?

A

IgA

31
Q

Blood vs mucosal IgA, whats the difference?

A 
Blood = monomeric
Mucosal = dimeric, linked by a J chain
32
Q

What are the functions of secretory IgA?

A
  1. Binds to mucus layer coating the epithelial surface via carbohydrate determinants in secretory component, this binding allows:
    - Prevention of the adherence of microorganisms
    - Neutralisation of microbial toxins and enzymes
  2. Limits access of pathogens to the mucosal surfaces, without risking inflammatory damage to the tissue as it has little capacity to active he complement pathway or act as an opsonin (cannot induce inflammation)
  3. Important role in symbiotic relationship between individual and their commensal bacteria, helping to restrict these organisms to the gut lumen
33
Q

In IgA deficient patients, which antibody replaces its role?

A

Secretory IgM

34
Q

What are the important tasks of the mucosal immune system (MALT)?

A
  1. Ignore harmless antigens

2. Mount protective immune responses to pathogens

35
Q

Why are there normally no adverse responses against food antigens and commensal flora?

A
  1. Food antigens
    - The default response to oral administration of a protein antigen is the development of specific peripheral unresponsiveness = oral tolerance
    - Antigen-specific effector T cells are turned off or deleted
    - Antigen-specific Treg cells are generated (anti-inflammatory)
  2. Commensals
    - Induce IgA and Treg cells in the intestine
    - Ignored by the systemic immune systems - common antigens normally dont reach the rest of the body - only PPs, isolated lymphoid follicles and mesenteric LNs recognise them
36
Q

If under physiological conditions, conditioned DCs at mucosal surfaces are immature/non-activated and favour the induction of tolerance, how does the immune system mount an efficient response when exposed to pathogens?

A

In the presence of pathogens, DCs become fully activated, and induce CD4+ T cells to differentiate to effectors

37
Q

How does the immune system distinguish between harmless commensals and pathogenic bacteria?

A
  1. The TLR4 is expressed at the base of crypts where you wont really see many commensals
  2. TLR5 is expressed on the basolateral side of the intestinal epithelium (facing the lamina propria) this means that pathogens invading tissues can trigger TLR activation whereas commensals sitting out in the mucus layer wont have access to TLRs
  3. Commensals have their own traits to avoid PRR activation, such as changes in flagellin sequence allows it to not bind as strongly to TLR5 (rendered hyporesponsive)

Gastrointestinal pathophysiology (22 decks)

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