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The Journal of Immunology, Vol 140, Issue 10 3324-3330, Copyright © 1988 by American Association of Immunologists
ARTICLES |
MK Jenkins, JD Ashwell and RH Schwartz
Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.
Stimulation of IL-2-producing T cell clones with chemically modified APC and Ag induces a state of proliferative unresponsiveness, i.e., subsequent stimulation with normal APC and Ag fails to elicit IL-2 production. One possible effect of chemical modification on the APC is the destruction of its ability to provide costimulatory signals. To test this, various potential costimulators were added to T cells at the time of exposure to Ag and chemically modified APC. None of the cytokines tested, including IL-1, had a positive effect; however, addition of allogeneic spleen cells allowed a T cell proliferative response and prevented the induction of subsequent unresponsiveness. Fractionation of the spleen cells showed that low density B cells and macrophages were the best source of costimulatory activity. Allogeneic resting B cells provided some costimulatory activity and resting T cells, none at all. Attempts to mimic costimulatory signals with the phorbol ester PMA were only partially successful. PMA prevented the induction of T cell unresponsiveness but failed to allow T cell proliferation in response to Ag plus chemically modified APC. Our results suggest that IL-2 production by normal T cell clones is dependent not only on T cell receptor occupancy, but also on short range costimulatory signals that are provided to different degrees by various non-T accessory cells.
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J. Sprent, E.-K. Gao, and S.R. Webb T-cell Tolerance to H-2 Molecules: Role of the Thymus Cold Spring Harb Symp Quant Biol, January 1, 1989; 54(0): 789 - 797. [Abstract] [PDF]
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M. Jenkins, R. Schwartz, and D. Pardoll Effects of cyclosporine A on T cell development and clonal deletion Science, September 23, 1988; 241(4873): 1655 - 1658. [Abstract] [PDF]
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