T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis

Jeffrey M. Critchfield, Michael K. Racke, Juan Carlos Zúñiga-Pflücker, Barbara Cannella, Cedric S. Raine, Joan Goverman, Michael J. Lenardo

Research output: Contribution to journalArticle

480 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1139-1143
Number of pages5
Issue number5150
StatePublished - Jan 1 1994


ASJC Scopus subject areas

  • General

Cite this

Critchfield, J. M., Racke, M. K., Zúñiga-Pflücker, J. C., Cannella, B., Raine, C. S., Goverman, J., & Lenardo, M. J. (1994). T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis. Science, 263(5150), 1139-1143. https://doi.org/10.1126/science.7509084