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DOI 10.1172/jci112459

Медицинская библиотека · The Journal of clinical investigation · 1986

Alterations in cytotoxic and helper T cell function after infection of T cell clones with human T cell leukemia virus, type I.

Yarchoan R, Guo H G, Reitz M, Maluish A, Mitsuya H, Broder S

СтатьяПоддержка службы здравоохранения СШАПеревод пока не подготовлен

Аннотация

HTLV-I is a transforming human retrovirus that is an etiologic agent of adult T cell leukemia/lymphoma. To investigate the effects of this virus on T cell functions, two OKT3+, OKT4+, OKT8- cytotoxic clones (8.7 and 8.8) specific for allogeneic cells bearing DPw2, a class II histocompatibility antigen, were studied before and after infection with HTLV-I. The clones retained cytotoxic function for up to 70 d after exposure to HTLV-I, even without subsequent antigenic stimulation, but then lost their cytotoxic activity. Prior to infection with HTLV-I, clone 8.8 also lysed OKT3 hybridoma cells; after infection, cytotoxic activity against these OKT3-antibody bearing cells was lost in parallel with the loss of activity against DPw2-bearing target cells. In addition, expression of T3 surface antigen by HTLV-I-infected 8.8 cells was decreased at a time when they lost their cytotoxic activity, possibly contributing to the loss of cytotoxic function. Finally, clone 8.8 could provide help for nonspecific IgG production by autologous B cells when stimulated with irradiated DPw2-bearing non-T cells. After infection with HTLV-I, this helper function became independent of DPw2-stimulation and persisted even when the cytotoxic activity was lost. An OKT4+ T cell clone thus could simultaneously manifest both cytotoxic and helper T cell activities, and these activities were differentially affected after HTLV-I infection.

Для цитирования: Yarchoan R, Guo H G, Reitz M, Maluish A, Mitsuya H, Broder S. Alterations in cytotoxic and helper T cell function after infection of T cell clones with human T cell leukemia virus, type I.. The Journal of clinical investigation. 1986. DOI: 10.1172/jci112459.

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