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Department of Immunology, Weizmann Institute of Science, Rehovot, Israel
LPS, a molecule produced by Gram-negative bacteria, is known to activate both innate immune cells such as macrophages and adaptive immune B cells via TLR4 signaling. Although TLR4 is also expressed on T cells, LPS was observed not to affect T cell proliferation or cytokine secretion. We now report, however, that LPS can induce human T cells to adhere to fibronectin via TLR4 signaling. This response to LPS was confirmed in mouse T cells; functional TLR4 and MyD88 were required, but T cells from TLR2 knockout mice could respond to LPS. The human T cell response to LPS depended on protein kinase C signaling and involved the phosphorylation of the proline-rich tyrosine kinase (Pyk-2) and p38. LPS also up-regulated the T cell expression of suppressor of cytokine signaling 3, which led to inhibition of T cell chemotaxis toward the chemokine stromal cell-derived factor 1
(CXCL12). Thus, LPS, through TLR4 signaling, can affect T cell behavior in inflammation.
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 on LPS was supported in part by grants from the Minerva Foundation (Germany), the Israeli Science Foundation administered by the Israel Academy of Sciences and Humanities (Grant 1036/03) (to O.L.), the European Union’s Fifth Framework Program (FP5), and the Israel Lung Association.
2 A.Z.-Z. and G.T.-L. contributed equally to this study.
4 Address correspondence and reprint requests to Prof. Irun R. Cohen, Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel. E-mail address: irun.cohen{at}weizmann.ac.il
5 Abbreviations used in this paper: siRNA, silent RNA; FN, fibronectin; Pyk-2, proline-rich tyrosine kinase 2; SDF, stromal cell-derived factor; SOCS, suppressor of cytokine signaling.
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