T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis
JM Critchfield, MK Racke, JC Zúñiga-Pflücker… - Science, 1994 - science.org
JM Critchfield, MK Racke, JC Zúñiga-Pflücker, B Cannella, CS Raine, J Goverman…
Science, 1994•science.orgEncounters 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 …
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 …
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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