Reports

T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis

Science  25 Feb 1994:
Vol. 263, Issue 5150, pp. 1139-1143
DOI: 10.1126/science.7509084

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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