IMM2022 Study Guide - Final Guide: Segmented Filamentous Bacteria, Lacrimal Gland, Lamina Propria
4 May 2018
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Diet and the immune system
Mucosal tissues include the urogenital tract,
kidney and lachrymal gland.
Anatomical features of mucosal IMM include
• Peyers patches
• Isolated lymphoid follicles
• Tonsils
• Specialised antigen uptake cells M
cells in peyers patches
EFFECTOR MECHANISMS
Note that there is activated memory T even
in the absence of infection. Epithelial layer in
the gut has tight junctions and secretes
defensins (physical and chemical barrier)
You do not see neutrophils in gut unless there
is an infection.
You do see: CD4, macrophage, CD8 (in
epithelium), DC, IgA, mas, plasma all in the
lamina propria.
MICROFIELD CELLS (M-CELLS)
These transport antigens from gut lumen
peyers patches. They endocytosis or
pinocytose antigens. Activated T can then
facilitate class switching in B to IgA.
SECRETORY (DIMER) IgA
Has a J-chain and secretory component. The J-
chain helps it not be broken down in the
acidic environment in the gut. Dimeric IgA is
transported into the gut lumen through
epithelial cells at the base of crypts. IgA is
secreted in response to resident microbiota.
Secretory IgA is neutralising. It does not act on
an opsin or activate complement. They do not
cause inflammation. IgA can export toxins and
pathogens from the LP whilst being secreted.
Binding of IgA to dectin-1 on M-cells allows
transport of antigen to DC-SIGN+ IL-10
production anti inflamm. This stops
commensals for being invasive.
Note that mucosal surfaces are thins and
permeable.
Note that cytokines BAFF and APIRL promote
IgA switching.
IMM VS TOLERANCE
Protective immunity: invasive bacteria,
viruses, toxins intestinal IgA, specific Ab
present in serum local and systemic
effector and memory T cells enhanced
memory response.
Mucosal tolerance: food proteins, commensal
bacteria some local IgA, low or no Ab in
serum no local effect T-cell response
low or no response
GUT MICROBIOTA are beneficial
• Firmicutes spp.
• Bacteroidetes spp.
• All commensals are specific to
ecological niches.
Due to co-evolution – we tolerate these. They
have roles in digestion, metabolism, vitamin
synthesis, digestion of dietary fibre.
Tolerance: continual LPs exposure (a PAMP)
helps maintain anti-inflamm through
regulation of NF-KB.
GUT EPITHELIUM
• M-cells
• Goblet mucin production
• Paneth antimicrobial proteins
Resident microbiota Th17 and IL-22
response tightens junctions of epithelial
cells; also acts on epithelium to produce
defensins (poke holes in bacteria) it is all
about balance as this can damage good
bacteria too
Good balance = physiological inflammation
can come from commensals activating TLRs
IgA retain bacteria in mucus.
SEGMENTED FILAMENTOUS BACTERIA is
important in maintaining physiological
inflammation
• Interacts with epithelium directly
• Th1 and TH17 response epithelium
integrity is promoted
Document Summary
Mucosal tissues include the urogenital tract, kidney and lachrymal gland. Isolated lymphoid follicles: peyers patches, tonsils, specialised antigen uptake cells m cells in peyers patches. Protective immunity: invasive bacteria, viruses, toxins intestinal iga, specific ab present in serum local and systemic effector and memory t cells enhanced memory response. Mucosal tolerance: food proteins, commensal bacteria some local iga, low or no ab in serum no local effect t-cell response low or no response. Note that there is activated memory t even in the absence of infection. Epithelial layer in the gut has tight junctions and secretes defensins (physical and chemical barrier) You do not see neutrophils in gut unless there is an infection. You do see: cd4, macrophage, cd8 (in epithelium), dc, iga, mas, plasma all in the lamina propria. These transport antigens from gut lumen peyers patches. Activated t can then facilitate class switching in b to iga.
