T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis

Jeffrey M. Critchfield; Michael K. Racke; Juan Carlos Zúñiga-Pflücker; Barbara Cannella; Cedric S. Raine; Joan Goverman; Michael J. Lenardo

doi:10.1126/science.7509084

T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis

Jeffrey M. Critchfield, Michael K. Racke, Juan Carlos Zúñiga-Pflücker, Barbara Cannella, Cedric S. Raine, Joan Goverman, Michael J. Lenardo

Pathology

Research output: Contribution to journal › Article › peer-review

505 Scopus citations

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.

Original language	English (US)
Pages (from-to)	1139-1143
Number of pages	5
Journal	Science
Volume	263
Issue number	5150
DOIs	https://doi.org/10.1126/science.7509084
State	Published - 1994

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title = "T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis",

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.",

author = "Critchfield, {Jeffrey M.} and Racke, {Michael K.} and Z{\'u}{\~n}iga-Pfl{\"u}cker, {Juan Carlos} and Barbara Cannella and Raine, {Cedric S.} and Joan Goverman and Lenardo, {Michael J.}",

year = "1994",

doi = "10.1126/science.7509084",

language = "English (US)",

volume = "263",

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T1 - T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis

AU - Critchfield, Jeffrey M.

AU - Racke, Michael K.

AU - Zúñiga-Pflücker, Juan Carlos

AU - Cannella, Barbara

AU - Raine, Cedric S.

AU - Goverman, Joan

AU - Lenardo, Michael J.

PY - 1994

Y1 - 1994

N2 - 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.

AB - 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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ER -

T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis

Abstract

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