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 journalArticlepeer-review

505 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 - 1994

ASJC Scopus subject areas

  • General


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