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J. Exp. Med.,
Volume 187, Number 2, January 19, 1998 177-183
By
From the Institut Necker, Institut National de la Santé et de la Recherche Médicale 373, F-75730
Paris, Cedex 15, France
Continuous antigenic stimulation in vivo can result in the generation of so-called "anergic"
CD4+ or CD8+ T cells that fail to proliferate upon antigenic stimulation and fail to develop
cytolytic effector functions. Here we show that class II major histocompatibility complex-restricted
T cells specific for influenza hemagglutinin (HA) that become anergic in mice expressing HA
under control of the immunoglobulin
promoter exhibit an impaired effector function in
causing diabetes in vivo, as compared to their naive counterparts, when transferred into immunodeficient recipients expressing HA under the control of the insulin promoter. Furthermore,
HA-specific T cells anergized in vivo contain higher levels of interleukin (IL)-4 messenger
RNA (mRNA) than naive and recently activated T cells with the same specificity and more than a 100-fold higher levels of IL-10 mRNA. The higher expression of the IL-10 gene is also
evident at the protein level. These findings raise the interesting possibility that T cells rendered anergic in vivo have in fact become regulatory T cells that may influence neighboring immune
responses through the release of IL-10.
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