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30 Cards in this Set
- Front
- Back
- 3rd side (hint)
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What is MALT? |
Mucosa-associated lymphatic system |
It's a system |
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What are the parts of MALT? |
BALT, MALT of the urogenital system, GALT, NALT, Skin duct/exocrine glands |
There's five of them |
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What influences the mucosal immune system? |
Maternal stress, feeding practices, microbiome, vaccination, nutrition, infection, host of antigens encountered |
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What is the MALT tissue-centered network centralised around? |
Single cell epithelium |
Type/thickness of epithelium |
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Form and function of villi |
Get shorter and broader from start of small intestine to caecum (no villi, just crypts) |
Length and thickness change |
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Form and function of goblet cells |
Discontinuous mucous layer in SI reflects absorptive requirements; goblet cells become more numerous progressing down to LI |
Change in number |
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Form and function or AMPs and IgA |
Crypts enriched with Paneth cells secreting AMPs, which crosslink with mucous layer |
Paneth cells |
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Form and function of caecum |
Start of LI; reservoir for commensal bacteria that are fermentative and digest complex carbs that aren't broken down in SI |
Enzymes |
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Form and function of large intestine |
No villi in colon, crypts smaller; thick, continuous layer helps compartmentalise bacteria |
Villi and crypts |
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List specialised intestinal epithelial cells |
M cells, Goblet cells, Peyer's patches, Paneth cells, enterocytes, colonocytes |
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What are some gut-associated lymphoid tissues? |
Tonsils, adenoids, Peyer's patches, mesenteric lymph nodes (MLN), isolated lymphoid follicles, diffuse scattering of immune cells |
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What's the role of M cells? |
Deliver antigen to APCs and Peyer's patch by endocytosis and phagocytosis |
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What is the key site for oral tolerance induction? |
Mesenteric lymph nodes (MLNs) - lymphocytes acquire a4B6 (via RA) which permits entry into gut |
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What must be present for dendritic cell activation? |
PAMPs or DAMPs |
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Name the two mucosal lymphocytes in MALT |
Lamina Propria (LP) and Intraepithelial lymphocytes (IEL) (type A 'inducible' and type B 'natural') |
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Which two cells sample antigen at the gut lumen? |
Mucosal CX3CR1 macrophages and CD103+ (a4B7) myeloid DCs |
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Define immune exclusion |
Promotion of antigen and pathogen clearance by sIgA, by blocking access to epithelial receptors, entrapping them in mucous and facilitating their removal |
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Why is IgA important to mucosal health? |
Constantly traffics to lumen to eliminate pathogens, inhibits binding/invasion of microbiome; antigen complexed to IgA transported back via same mechanism; class switching |
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What is oral tolerance? |
A case of peripheral tolerance. Continuous and natural, driven by oral antigen; results in systemic and mucosal antigen-specific long-lived protection |
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List the processes involved in immune priming for oral tolerance |
Ignorance, anergy, clonal deletion, Tregs, antigen dose and location, microbiome-dependent effects |
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Which two vitamins are involved in oral tolerance? |
Vitamin A and Vitamin D |
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Which disease may be immune-mediated but not classically autoimmune? |
Inflammatory bowel disease |
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Outline the structure of the microbiome |
Taxonomic layers, each phylum (four main divisions) containing different genera (genuses) |
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Outline the composition of the microbiota |
Predominant phyla = Firmicutes + Bacteroidetes, followed by Actinobacteria + Verrucomicrobia |
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Outline the functions of the microbiota |
Produce anti-inflammatory compounds, teach immune system how to recognise invaders, break down food, produce vitamins and metabolites |
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What is the primary cause of dysbiosis? |
Overuse of antibiotics, change in diet, elimination of beneficial organisms that work with the microbiota (e.g. nematodes) |
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What is the primary outcome of dysbiosis? |
Reduced diversity, shifts in and/or manipulation of phyla, linked to chronic inflammatory diseases |
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What happens when barrier integrity is compromised? |
Endotoxemia --> Systemic inflammation --> Compromised oral tolerance |
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Describe the TLR4 pattern recognition mechanism |
Helps in microbiota tolerance. Low luminal levels, weakly responsive to LPS, mostly intracellular in Golgi apparatus, surface TLR ligation causes tightening of epithelial junctions enhancing barrier but not inflammation |
Microbiota |
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Describe the TLR9 pattern recognition mechanism |
Luminal stimulation leads to anti-inflammatory signalling via ikB-a --> Prevents NF-kB proinflammatory signalling Basolateral TLR9 activation degrades ikB-a --> Permits NF-kB proinflammatory signalling |
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