Regulatory T cells control autoimmunity in vivo by inducing apoptotic depletion of activated pathogenic lymphocytes.
J Immunol
; 170(6): 2985-92, 2003 Mar 15.
Article
en En
| MEDLINE
| ID: mdl-12626551
ABSTRACT
Clinical autoimmunity requires both activation of self-reactive T cells as well as a failure of peripheral tolerance mechanisms. We previously identified one such mechanism that involves regulatory T cells recognizing TCR V beta 8.2 chain-derived peptides in the context of MHC. How this regulation affects the fate of target V beta 8.2(+) T lymphocytes in vivo that mediate experimental autoimmune encephalomyelitis has remained unknown. The present study using immunoscope and CFSE-labeling analysis demonstrates that the expansion of regulatory CD4 and CD8 T cells in vivo results in apoptotic depletion of the dominant, myelin basic protein-reactive V beta 8.2(+) T cells, but not subdominant V beta 13(+) T cells. The elimination of only activated T cells by this negative feedback mechanism preserves the remainder of the naive V beta 8.2(+) T cell repertoire and at the same time results in protection from disease. These studies are the first in clearly elucidating the fate of myelin basic protein-specific encephalitogenic T cells in vivo following regulation.
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Banco de datos:
MEDLINE
Asunto principal:
Activación de Linfocitos
/
Subgrupos de Linfocitos T
/
Depleción Linfocítica
/
Apoptosis
/
Encefalomielitis Autoinmune Experimental
Límite:
Animals
Idioma:
En
Revista:
J Immunol
Año:
2003
Tipo del documento:
Article
País de afiliación:
Estados Unidos