Publication Date:
1994-02-25
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Critchfield, J M -- Racke, M K -- Zuniga-Pflucker, J C -- Cannella, B -- Raine, C S -- Goverman, J -- Lenardo, M J -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1139-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7509084" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Antigens/*immunology
;
Apoptosis
;
CD4-Positive T-Lymphocytes/*immunology
;
Cell Division
;
Cells, Cultured
;
Cytochrome c Group/immunology
;
Dose-Response Relationship, Immunologic
;
Encephalomyelitis, Autoimmune, Experimental/*immunology/pathology/therapy
;
*Immune Tolerance
;
Immunotherapy
;
Interleukin-2/immunology/pharmacology
;
Lymphocyte Activation
;
Mice
;
Mice, Transgenic
;
Myelin Basic Protein/immunology
;
Myelin Sheath/immunology/pathology
;
Spinal Cord/pathology
;
T-Lymphocytes/*immunology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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