T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis
摘要：
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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关键词：
Animals Mice T-Lymphocytes CD4-Positive T-Lymphocytes Spinal Cord Myelin Sheath Cells, Cultured Encephalomyelitis, Autoimmune, Experimental Cytochrome c Group Myelin Basic Proteins
DOI：
10.1126/science.7509084
被引量：
年份：
1994
Taylor & Francis
Wiley
万方医学
JSTOR
NCBI
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