Toll-like receptors and immune regulation:: their direct and indirect modulation on regulatory CD4+ CD25+ T cells

被引：136

作者：

Liu, Guangwei ^{[1
]}

Zhao, Yong ^{[1
]}

机构：

[1] Chinese Acad Sci, Inst Zool, State Key Lab Biomembrane & Membrane Biotechnol, Transplantat Biol Res Div, Beijing, Peoples R China

来源：

IMMUNOLOGY | 2007年 / 122卷 / 02期

关键词：

Toll-like receptors; regulatory CD4(+); CD25(+); T cells; immune response; immune tolerance; autoimmune disease;

D O I：

10.1111/j.1365-2567.2007.02651.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：

Regulatory CD4(+) CD25(+) T (Treg) cells with the ability to suppress host immune responses against self- or non-self antigens play important roles in the processes of autoimmunity, transplant rejection, infectious diseases and cancers. The proper regulation of CD4(+) CD25(+) Treg cells is thus critical for optimal immune responses. Toll-like receptor (TLR)-mediated recognition of specific structures of invading pathogens initiates innate as well as adaptive immune responses via antigen-presenting cells (APCs). Interestingly, new evidence suggests that TLR signalling may directly or indirectly regulate the immunosuppressive function of CD4(+) CD25(+) Treg cells in immune responses. TLR signalling may shift the balance between CD4(+) T-helper cells and Treg cells, and subsequently influence the outcome of the immune response. This immunomodulation pathway may therefore have potential applications in the treatment of graft rejection, autoimmune diseases, infection diseases and cancers.

引用

页码：149 / 156

页数：8

共 79 条

[1] Inhibition of phosphoinositide 3-kinase enhances TRIF-dependent NF-κB activation and IFN-β synthesis downstream of Toll-like receptor 3 and 4 [J].