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Rheumatology Advance Access originally published online on June 24, 2007
Rheumatology 2007 46(10):1525-1530; doi:10.1093/rheumatology/kem154
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

REVIEWS

Altered signal transduction in SLE T cells

K. Tenbrock1, Y.-T. Juang2, V. C. Kyttaris2 and G. C. Tsokos2

1Department of Pediatrics, Division of Rheumatology, University Hospital Muenster, 48145 Muenster, Germany and 2Division of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.

Correspondence to: Klaus Tenbrock, University of Münster, Department of Pediatrics, Division of Rheumatology, Institute of Experimental Dermatology, Röntgenstr. 21 D-48149 Münster, Germany. E-mail: ktenbroc{at}uni-muenster.de


  Abstract

T cells from patients with systemic lupus erythematosus display numerous signalling abnormalities. The T cell receptor complex is rewired with the common FcR{gamma} chain replacing the CD3 {zeta} chain while the T cell surface membrane lipid rafts are aggregated. These two aberrations result in enhanced early signalling events and altered downstream signalling events. These are in turn responsible for an altered expression of cytokines such as interleukin-6 (IL-6), IL-10, IL-2, IFNy and CD40 ligand. While some of these abnormalities explain the enhanced ability of T cells to help B cells to produce autoantibodies, decreased IL-2 production results in enhanced susceptibility to infections, reduced activation-induced cell death and prolonged survival of autoreactive T cells, which promote help to autoreactive B cells.

KEY WORDS: lupus, CREM, CamKIV, Elf-1, NFAT, AP-1

Submitted 30 January 2007; revised version accepted 3 May 2007.
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