Abstract
Encounters with antigen can stimulate T cells to become activated and proliferate, become nonresponsive to antigen, or to die. T cell death was shown to be a physiological response to interleukin-2-stimulated cell cycling and T cell receptor reengagement at high antigen doses. This feedback regulatory mechanism attenuates the immune response by deleting a portion of newly dividing, antigen-reactive T cells. This mechanism deleted autoreactive T cells and abrogated the clinical and pathological signs of autoimmune encephalomyelitis in mice after repetitive administration of myelin basic protein.
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Dates
Type | When |
---|---|
Created | 18 years, 10 months ago (Oct. 5, 2006, 8:01 p.m.) |
Deposited | 1 year, 7 months ago (Jan. 14, 2024, 11:04 p.m.) |
Indexed | 1 month, 2 weeks ago (July 14, 2025, 11:42 p.m.) |
Issued | 31 years, 6 months ago (Feb. 25, 1994) |
Published | 31 years, 6 months ago (Feb. 25, 1994) |
Published Print | 31 years, 6 months ago (Feb. 25, 1994) |
@article{Critchfield_1994, title={T Cell Deletion in High Antigen Dose Therapy of Autoimmune Encephalomyelitis}, volume={263}, ISSN={1095-9203}, url={http://dx.doi.org/10.1126/science.7509084}, DOI={10.1126/science.7509084}, number={5150}, journal={Science}, publisher={American Association for the Advancement of Science (AAAS)}, author={Critchfield, Jeffrey M. and Racke, Michael K. and Zúñiga-Pflücker, Juan Carlos and Cannella, Barbara and Raine, Cedric S. and Goverman, Joan and Lenardo, Michael J.}, year={1994}, month=feb, pages={1139–1143} }