Toll-like receptor 4 signaling in T cells promotes autoimmune inflammation
Toll-like receptor 4 signaling in T cells promotes autoimmune inflammation
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DOI：
10.1073/pnas.1120585109
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发表时间：
2012-08-07
影响因子：
11.1
通讯作者：
Dong, Chen
中科院分区：
文献类型：
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作者：
Reynolds, Joseph M.;Martinez, Gustavo J.;Dong, Chen
Toll-like receptors (TLRs) are critical components of innate immunity and function as rapid pathogen sensors. TLR4 is expressed on CD4(+) T cells as well, the functional significance of which is unclear. In this study, we analyzed the function of TLR4 in T cells but did not find a role in promoting T helper (Th) cell polarization. Instead, TLR4 ligation enhanced both CD4(+) T-cell proliferation and survival in vitro. Using the experimental autoimmune encephalomyelitis (EAE) model, we found that the loss of TLR4 solely in CD4(+) T cells almost completely abrogated disease symptoms, mainly through blunted Th17 and, to a lesser degree, Th1 responses. Moreover, Tlr4(-/-) gamma delta T cells were defective in IL-17 and IFN-gamma production following EAE induction. This study supports an important role of this innate receptor in the direct regulation of T-cell activation and survival during autoimmune inflammation.
