|
|
|
|
|
|
|
||
J. Exp. Med.,
Volume 187, Number 1, January 5, 1998 89-96
By
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.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
| TABLE OF CONTENTS |
|
