Page 668 - Veterinary Immunology, 10th Edition

Enterocytes express receptors for many microbial-associated
VetBooks.ir molecular patterns (MAMPs) including TLRs-1, -2, -3, -5, and -9 as

well as NOD-2. When exposed to MAMPs, recruitment of MyD88
and TRIF result in NF-κB and MAP kinase activation and cytokine

synthesis. In practice, bacterial signals trigger the production of
some antimicrobial peptides and cytokines but not inflammation.
This is because the PRRs are not expressed on the luminal side of
enterocytes, where they would normally come into contact with

commensals. They are located at the base of the cells and at
intracellular locations. Thus they are activated only after bacteria
penetrate the epithelial barrier. By preventing microbial invasion,
enterocytes also prevent the development of inflammation within

the intestinal wall. Some of the cytokines produced by enterocytes
influence the regulatory activities of antigen-processing cells such
as macrophages and dendritic cells. IL-10 inhibits the TLR-MyD88
pathway, whereas IL-2 inhibits TLR-independent pathways.

The antimicrobial peptides within the inner mucus layer keep
most of the microbiota from contacting the enterocytes and thus
ensure that the microbiota remain within the intestinal lumen. They
not only protect the host from microbial invasion but also from the

potentially harmful inflammatory response that would occur when
MAMPs are absorbed into the body (Chapter 22).

ILC3 Cells

Group 3 innate lymphoid cells also regulate the interactions
between the microbiota and its host (Fig. 19.4). They respond to IL-
23, IL-1β, and TSLP from dendritic cells by producing IL-17 and IL-
22. These attract neutrophils and promote the production of
antimicrobial peptides, especially REGIIIγ in the small intestine.

REGIIIγ interacts with the mucus layer to maintain a relatively
bacteria-free zone adjacent to the mucosal surface. ILC3 cells also
activate B cells and induce IgA production. They can promote

tolerance to food antigens by producing GM-CSF that in turn
promotes Treg production. Their production is regulated by the
aryl hydrocarbon receptor (Box 21.1).

Box 21.1

668