Toll-like receptor signaling and regulation of intestinal immunity

被引:64
作者
Kamdar, Karishma [1 ]
Vivien Nguyen [1 ,2 ]
DePaolo, R. William [1 ]
机构
[1] Univ So Calif, Keck Sch Med, Dept Microbiol & Immunol, Los Angeles, CA 90033 USA
[2] Childrens Hosp Los Angeles, Dept Pediat Gastroenterol & Nutr, Los Angeles, CA 90027 USA
关键词
TLR; intestine; mucosal immunity; commensal microbiota; inflammation; tolerance; EPITHELIAL-CELLS; DENDRITIC CELLS; GUT MICROBIOTA; GENE-EXPRESSION; LAMINA PROPRIA; RETINOIC ACID; T-CELLS; RESPONSES; INFLAMMATION; RECOGNITION;
D O I
10.4161/viru.23354
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The intestine is a complex organ that must maintain tolerance to innocuous food antigens and commensal microbiota while being also able to mount inflammatory responses against invading pathogenic microorganisms. The ability to restrain tolerogenic responses while permitting inflammatory responses requires communication between commensal bacteria, intestinal epithelial cells and immune cells. Disruption or improper signaling between any of these factors may lead to uncontrolled inflammation and the development of inflammatory diseases. Toll-like receptors (TLR) recognize conserved molecular motifs of microorganisms and, not surprisingly, are important for maintaining tolerance to commensal microbiota, as well as inducing inflammation against pathogens. Perturbations in individual TLR signaling can lead to a number of different outcomes and illustrate a system of regulation within the intestine in which each TLR plays a largely non-redundant role in mucosal immunity. This review will discuss recent findings on the roles of individual TLRs and intestinal homeostasis.
引用
收藏
页码:207 / 212
页数:6
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