Functional aspects of Toll-like receptor/MyD88 signalling during protozoan infection: focus on Toxoplasma gondii

被引：45

作者：

Egan, C. E. ^{[1
]}

Sukhumavasi, W. ^{[1
]}

Butcher, B. A. ^{[1
]}

Denkers, E. Y. ^{[1
]}

机构：

[1] Cornell Univ, Coll Vet Med, Dept Microbiol & Immunol, Ithaca, NY 14853 USA

来源：

CLINICAL AND EXPERIMENTAL IMMUNOLOGY | 2009年 / 156卷 / 01期

关键词：

infection; -; protozoan; innate immunity; Toll-like receptor; NF-KAPPA-B; MYELOID DIFFERENTIATION FACTOR-88; INFLAMMATORY-BOWEL-DISEASE; CELL-MEDIATED-IMMUNITY; DENDRITIC CELLS; HOST-RESISTANCE; CUTTING EDGE; TRYPANOSOMA-CRUZI; SMALL-INTESTINE; ORAL INFECTION;

D O I：

10.1111/j.1365-2249.2009.03876.x

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Toll-like receptor (TLR)/MyD88 signalling has emerged as a major pathway of pathogen recognition in the innate immune system. Here, we review recent data that begin to show how this pathway controls the immune response to protozoan infection, with particular emphasis on the opportunistic pathogen Toxoplasma gondii. The various ways that the parasite activates and suppresses TLR/MyD88 signalling defines several key principals that illuminate the complexities of the host-pathogen interaction. We also speculate how TLR/MyD88 signalling might be exploited to provide protection against Toxoplasma, as well as other protozoa and infection in general.

引用

页码：17 / 24

页数：8

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