The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/1/89/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 1, January 5, 1998 89-96

Article

Persistence of Peptide-induced CD4+ T cell Anergy In Vitro

Kelli R. Ryan and Brian D. Evavold

From the Department of Microbiology and Immunology, Emory University, Atlanta, Georgia 30322

Clonal T cell unresponsiveness, or anergy, has been proposed as a mechanism of peripheral tolerance in vivo, and as a potential means of curbing unwanted T cell responses. In this study, anergy was induced in a T helper cell (Th) clone reactive to hemoglobin (Hb) peptide 64–76 by coculture of the T cells with live antigen-presenting cells (APCs) and 74L, a peptide analog of Hb(64–76) that contains a single amino acid substitution of leucine for glycine at position 74, or with a low concentration of the agonist ligand. The anergic state was characterized by blunted proliferation and interleukin (IL) 2 production upon restimulation with Hb(64–76), and was not the result of impaired TCR/CD3 downmodulation. The addition of exogenous IL-12 transiently restored proliferation of the anergic lines, but removal of IL-12 from culture returned the T cells to their nonproliferative state. Interestingly, persistence of the anergic phenotype was observed despite biweekly restimulation with antigen, APCs, and IL-2. Thus, T cell unresponsiveness induced by a peptide produced a stable, persistent anergic state in a Th0 clone that was not reversible by stimulation with IL-2 or -12.

Address correspondence to Dr. Brian D. Evavold, Department of Microbiology and Immunology, Emory University, 1510 Clifton Rd., Atlanta, GA 30322. Phone: 404-727-3393; FAX: 404-727-3659; E-mail: evavold{at}microbio.emory.edu

A portion of this paper was presented as a poster entitled "Long-term Maintenance of T Cell Anergy by a Peptide Analog" at the Keystone Symposia on Tolerance and Autoimmunity on 15 April 1997.

1 Abbreviation used in this paper: wt, wild-type.


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