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Cutting Edge: TLR2 Directly Triggers Th1 Effector Functions
Author(s) -
Takayuki Imanishi,
Hiromitsu Hara,
Shinobu Suzuki,
Nobutaka Suzuki,
Shizuo Akira,
Takashi Saito
Publication year - 2007
Publication title -
the journal of immunology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.178.11.6715
Subject(s) - effector , microbiology and biotechnology , tlr2 , biology , acquired immune system , innate immune system , t cell receptor , t cell , stimulation , receptor , signal transduction , immunology , immune system , tlr4 , neuroscience , biochemistry
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-gamma 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.

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