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

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.

Keywords

Experimental autoimmune encephalomyelitisAntigenImmunologyImmune systemT cellMyelinMyelin basic proteinEncephalomyelitisBiologyCell biologyMultiple sclerosisNeuroscienceCentral nervous system

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Publication Info

Year: 1994
Type: article
Volume: 263
Issue: 5150
Pages: 1139-1143
Citations: 524
Access: Closed

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APA Style

                            
                                
                                    Jeffrey M. Critchfield, 
                                
                                    Michael K. Racke, 
                                
                                    Juan Carlos Zúñiga‐Pflücker
                                
                                et al.
                            
                            (1994). 
                            T Cell Deletion in High Antigen Dose Therapy of Autoimmune Encephalomyelitis. 
                            Science
                            , 263
                            (5150)
                            , 1139-1143.
                            https://doi.org/10.1126/science.7509084
                        

Identifiers

DOI: 10.1126/science.7509084