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Science 25 February 1994: Vol. 263. no. 5150, pp. 1139 - 1143 DOI: 10.1126/science.7509084
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Articles
Science, Vol 263, Issue 5150, 1139-1143
Copyright © 1994 by American Association for the Advancement of Science
T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis
JM Critchfield,
MK Racke,
JC Zuniga-Pflucker,
B Cannella,
CS Raine,
J Goverman,
and
MJ Lenardo
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
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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