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International Immunology Advance Access originally published online on August 7, 2006
International Immunology 2006 18(10):1413-1419; doi:10.1093/intimm/dxl074
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© The Japanese Society for Immunology. 2006. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Peptide p277 of HSP60 signals T cells: inhibition of inflammatory chemotaxis

Gabriel Nussbaum*, Alexandra Zanin-Zhorov*, Francisco Quintana, Ofer Lider** and Irun R. Cohen

Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel

Correspondence to: I. R. Cohen; E-mail: irun.cohen{at}weizmann.ac.il

Peptide p277 is a 24-amino acid fragment of the heat shock protein 60 molecule, first discovered to be an antigen for diabetogenic T-cell clones in non-obese diabetic (NOD) mice. Therapeutic vaccination with p277 can arrest the spontaneous diabetogenic process both in NOD mice and in humans associated with a Th1 to Th2 cytokine shift specific for the autoimmune T cells. We now report that p277 can directly signal human T cells via innate toll-like receptor (TLR)-2, leading to up-regulation of integrin-mediated adhesion to fibronectin, and inhibition of chemotaxis to the chemokine SDF-1{alpha} in vitro. Resting CD45RA+ T cells responded to lower concentrations of p277 than resting CD45RO+ T cells, but activation of CD45RO+ T cells greatly increased their sensitivity to p277. Mouse T cells, but not macrophages, were also sensitive to the innate effects of peptide p277, and adoptive transfer of diabetes by splenic T cells from NOD mice could be inhibited by p277 treatment before transfer. Thus, T cells do respond innately to p277, and signaling by soluble p277 through TLR2 could contribute to the treatment of type 1 diabetes; p277 may stop the destruction of ß cells by signaling in concert both innate and adaptive receptors on T cells.

Keywords: chemotaxis, delayed-type hypersensitivity, toll-like receptors, type 1 diabetes mellitus

* These authors contributed equally to this study.

** Deceased.

Transmitting editor: L. Steinman


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