The Journal of Experimental Medicine
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Published online 10 February 2003 doi:10.1084/jem.20021633
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© Rockefeller University Press, 0022-1007/2003/2/403 $5.00
The Journal of Experimental Medicine, Volume 197, Number 4, 403-411

Regulatory T Cells Selectively Express Toll-like Receptors and Are Activated by Lipopolysaccharide

Iris Caramalho, Thiago Lopes-Carvalho, Dominique Ostler, Santiago Zelenay, Matthias Haury and Jocelyne Demengeot

Instituto Gulbenkian de Ciência, 2781-901 Oeiras, Portugal

Address correspondence to Jocelyne Demengeot, Instituto Gulbenkian de Ciência, Rua da Quinta Grande #6, Apartado 14, 2781-901 Oeiras, Portugal. Phone: 351-21-440-7908; Fax: 351-21-440-7970; E-mail: jocelyne{at}igc.gulbenkian.pt

Regulatory CD4 T cells (Treg) control inflammatory reactions to commensal bacteria and opportunist pathogens. Activation of Treg functions during these processes might be mediated by host-derived proinflammatory molecules or directly by bacterial products. We tested the hypothesis that engagement of germline-encoded receptors expressed by Treg participate in the triggering of their function. We report that the subset of CD4 cells known to exert regulatory functions in vivo (CD45RBlow CD25+) selectively express Toll-like receptors (TLR)-4, -5, -7, and -8. Exposure of CD4+ CD25+ cells to the TLR-4 ligand lipopolysaccharide (LPS) induces up-regulation of several activation markers and enhances their survival/proliferation. This proliferative response does not require antigen-presenting cells and is augmented by T cell receptor triggering and interleukin 2 stimulation. Most importantly, LPS treatment increases CD4+ CD25+ cell suppressor efficiency by 10-fold and reveals suppressive activity in the CD4+ CD45RBlow CD25- subset that when tested ex-vivo, scores negative. Moreover, LPS-activated Treg efficiently control naive CD4 T cell–dependent wasting disease. These findings provide the first evidence that Treg respond directly to proinflammatory bacterial products, a mechanism that likely contributes to the control of inflammatory responses.

Key Words: inflammation • tolerance • lymphocytes • regulation • innate immunity


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