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Science 25 February 1994:
Vol. 263. no. 5150, pp. 1139 - 1143
DOI: 10.1126/science.7509084

Articles

Science, Vol 263, Issue 5150, 1139-1143
Copyright © 1994 by American Association for the Advancement of Science


articles

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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Materials and Methods.
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J. Immunol. 160, 4441-4448
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Selective Induction of Apoptosis in Mature T Lymphocytes by Variant T Cell Receptor Ligands.
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Ovalbumin-Specific, MHC Class I-Restricted, {alpha}{beta}-Positive, Tc1 and Tc0 CD8+ T Cell Clones Mediate the In Vivo Inhibition of Rat IgE.
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Functional cleavage of the common cytokine receptor gamma  chain (gamma c) by calpain.
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