T-CELL DELETION IN HIGH ANTIGEN DOSE THERAPY OF AUTOIMMUNE ENCEPHALOMYELITIS

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 c ell cycling and T cell receptor reengagement at high antigen doses. Th is feedback regulatory mechanism attenuates the immune response by del eting a portion of newly dividing, antigen-reactive T cells. This mech anism deleted autoreactive T cells and abrogated the clinical and path ological signs of autoimmune encephalomyelitis in mice after repetitiv e administration of myelin basic protein.