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J. Exp. Med.,
Volume 188, Number 2, July 20, 1998 287-296
By
From the Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Bethesda, Maryland 20892
Peripheral tolerance may be maintained by a population of regulatory/suppressor T cells that
prevent the activation of autoreactive T cells recognizing tissue-specific antigens. We have previously shown that CD4+CD25+ T cells represent a unique population of suppressor T cells
that can prevent both the initiation of organ-specific autoimmune disease after day 3 thymectomy and the effector function of cloned autoantigen-specific CD4+ T cells. To analyze the
mechanism of action of these cells, we established an in vitro model system that mimics the
function of these cells in vivo. Purified CD4+CD25+ cells failed to proliferate after stimulation
with interleukin (IL)-2 alone or stimulation through the T cell receptor (TCR). When cocultured with CD4+CD25
cells, the CD4+CD25+ cells markedly suppressed proliferation by
specifically inhibiting the production of IL-2. The inhibition was not cytokine mediated, was
dependent on cell contact between the regulatory cells and the responders, and required activation of the suppressors via the TCR. Inhibition could be overcome by the addition to the cultures of IL-2 or anti-CD28, suggesting that the CD4+CD25+ cells may function by blocking
the delivery of a costimulatory signal. Induction of CD25 expression on CD25 T cells in vitro
or in vivo did not result in the generation of suppressor activity. Collectively, these data support the concept that the CD4+CD25+ T cells in normal mice may represent a distinct lineage
of "professional" suppressor cells.
chain (CD25)
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