Innate immunity in the small intestine.

PURPOSE OF REVIEW

In this article, we provide an update of the latest findings related to the innate immunity in the small intestine. In particular, we will focus on innate immune receptors and antimicrobial strategies that keep luminal bacteria and viral pathogens under control to avoid mucosal damage. These strategies include IgA secretion and antimicrobial peptides produced by Paneth cells, and downregulation or anergy of the innate immune receptors themselves.

RECENT FINDINGS

Pattern-recognition receptors are the main target in the study of innate immunity in the intestinal mucosa due to their involvement in the regulation of host-commensal interactions. It has been shown that TLR5-deficient mice develop metabolic syndrome and have altered intestinal microbiota. On the contrary, NOD2 has been associated with the activation of autophagy and the inhibition of TLR4. Moreover, NOD2 has been described to be essential to keep a feedback loop in the host-commensal homeostasis, through the kinase Rip-2.

SUMMARY

Innate immunity in the small intestine is mainly characterized by IgA secretion and Paneth cell antimicrobial function. In both cases pattern-recognition receptors, Toll-like receptors and nucleotide-binding and oligomerization domain-like receptors, are involved. A better understanding of the innate immunity in the small intestine would provide valuable information to develop vaccines against pathogens.