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A tumor-suppressor function for Fas (CD95) revealed in T cell-deficient mice.
Peng, S L; Robert, M E; Hayday, A C; Craft, J.
Afiliación
  • Peng SL; Section of Rheumatology, Yale University School of Medicine, New Haven, Connecticut, USA.
J Exp Med ; 184(3): 1149-54, 1996 Sep 01.
Article en En | MEDLINE | ID: mdl-9064331
Fas (CD95) and its ligand are central regulatory molecules in hematopoietic cells. Previous studies have suggested a role for Fas in the regulation of tumor progression, but Fas has not yet been conclusively identified as a tumor suppressor. Fas-deficient individuals lack malignant tumors, perhaps because of regulation by T cells. To investigate such a possibility, mice deficient in both T cells and Fas were generated, and they were found to develop severe B cell dysregulation characterized by malignant, lethal B cell lymphoma. Lymphoma arose from a monoclonal B220+CD19-CD5-CD23- B cell secreting immunoglobulin M, kappa rheumatoid factor. In contrast, animals containing alpha beta T cells, gamma delta T cells, and/or functional Fas suppressed the development of lymphoma. These data indicate that Fas functions as a tumor suppressor, and identifies roles for both alpha beta T cells and gamma delta T cells in Fas-independent tumor regulation.
Asunto(s)

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Linfocitos T / Receptor fas / Linfoma Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Exp Med Año: 1996 Tipo del documento: Article País de afiliación: Estados Unidos

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Linfocitos T / Receptor fas / Linfoma Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Exp Med Año: 1996 Tipo del documento: Article País de afiliación: Estados Unidos