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* Laboratory for Cell Signaling, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan;
Division of Molecular Mycology and Medicine, Center for Neurological Disease and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan;
Japan Society for the Promotion of Science and
Department of Host Defense, Research Institute for Microbial Disease, Osaka University, Osaka, Japan
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 TLRs on Th1 and Th2 effector cells and the molecular mechanisms underlying TLR-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 TLRs directly induced IFN-
production, 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.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by grants from the Ministry of Education, Culture, Sports, Science and Technology of Japan and the Japan Society for the Promotion of Science.
2 Current address: Department of Biomolecular Sciences, Faculty of Medicine, Saga University, Saga, Japan.
3 Current address: Nihon Schering K. K. Research Center, Kobe, Japan.
4 Address correspondence and reprint requests to Dr. Takashi Saito, Laboratory for Cell Signaling, RIKEN Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa, Japan 230-0045. E-mail address: saito{at}rcai.riken.jp
5 Abbreviations used in this paper: Pam3, N-palmitoyl-S-(2,3-bis(palmitoyloxy)-(2RS)-propyl)-Cys-Ser-Lys4; CsA, cyclosporin A; GADD, growth arrest and DNA damage; IRAK, IL-1R-associated kinase 4; MALP-2, macrophage-activating lipopeptide 2; MTS, 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium.
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