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*Joint Disorders
*Lyme Disease
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© The Rockefeller University Press, 0022-1007/1996/12/2109/ $5.00
The Journal of Experimental Medicine, Volume 184, Number 6, December 1, 1996 2109-2118

Articles

Apoptosis of Fashigh CD4+ Synovial T Cells by Borrelia-reactive Fas-ligandhigh {gamma}{delta} T Cells in Lyme Arthritis

Michael S. Vincent*, Karen Roessner*, David Lynch{ddagger}, David Wilson*, Sheldon M. Cooper*, Jurg Tschopp§, Leonard H. Sigal||, and Ralph C. Budd*

From the * Divisions of Immunobiology and Rheumatology, Department of Medicine, The University of Vermont College of Medicine, Burlington, Vermont 05405-0068; {ddagger} Immunex Corporation, Seattle, Washington 98101; § Institute of Biochemistry, University of Lausanne, Swiss Institute for Cancer Research, Epalinges, Switzerland; || Division of Rheumatology and Connective Tissue Research, Department of Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, New Jersey 08903

The function of the minor subset of T lymphocytes bearing the {gamma}{delta} T cell antigen receptor is uncertain. Although some {gamma}{delta} T cells react to microbial products, responsiveness has only rarely been demonstrated toward a bacterial antigen from a naturally occurring human infection. Synovial fluid lymphocytes from patients with Lyme arthritis contain a large proportion of {gamma}{delta} cells that proliferate in response to the causative spirochete, Borrelia burgdorferi. Furthermore, synovial {gamma}{delta} T cell clones express elevated and sustained levels of the ligand for Fas (APO-1, CD95) compared to {alpha}β T cells, and induce apoptosis of Fashigh CD4+ synovial lymphocytes. The findings suggest that {gamma}{delta} T cells contribute to defense in human infections, as well as manifest an immunoregulatory function at inflammatory sites by a Fas-dependent process.

Address correspondence to Dr. Ralph C. Budd, Division of Immunology, The University of Vermont College of Medicine, Given Medical Building Room C-303, Burlington, VT 05405-0068.

This work was supported by National Institutes of Health grant AR43520 and the Arthritis Foundation.

1Abbreviation used in this paper: PBL, peripheral blood lymphocytes.


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