Cutting edge: TLR2 directly triggers Th1 effector functions

被引:169
作者
Imanishi, Takayuki
Hara, Hiromitsu
Suzuki, Shinobu
Suzuki, Nobutaka
Akira, Shizuo
Saito, Takashi
机构
[1] RIKEN, Ctr Allergy & Immunol, Lab Cell Signaling, Tsurumi Ku, Yokohama, Kanagawa 2300045, Japan
[2] Nagoya Univ, Grad Sch Med, Ctr Neurol Dis & Canc, Div Mol Mycol & Med, Nagoya, Aichi 464, Japan
[3] Osaka Univ, Res Inst Microbial Dis, Japan Soc Promot Sci, Suita, Osaka 565, Japan
[4] Osaka Univ, Res Inst Microbial Dis, Dept Host Def, Suita, Osaka 565, Japan
关键词
D O I
10.4049/jimmunol.178.11.6715
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 receptors recognize pathogen-associated molecular patterns, activate innate immunity, and consequently modulate adaptive immunity in response to infections. TLRs are also expressed on T cells, and it has been shown that T cell activation is modulated by TLR ligands. However, the functions of Ms on Th1 and Th2 effector cells and the molecular mechanisms underlying M-mediated activation are not fully understood. We analyzed TLR functions and downstream signaling events in both effector T cells. In mouse Th1 cells the stimulation by TLR2 but not by other Ms directly induced IFN-gamma yproduction, cell proliferation, and cell survival without TCR stimulation, and these effects were greatly enhanced by IL-2 or IL-12 through the enhanced activation of MAPKs. In contrast, no TLR affected the function of effector Th2 cells. These results identify TLR2 as a new specific activator of Th1 cell function and imply the involvement in th1-mediated responses.
引用
收藏
页码:6715 / 6719
页数:5
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