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The interaction of interleukin 2 with its receptor in the generation of suppressor T cells in antigen-specific and antigen-nonspecific systems in vitro.
Oh-Ishi, T; Goldman, C K; Misiti, J; Waldmann, T A.
Afiliação
  • Oh-Ishi T; Metabolism Branch, National Cancer Institute, Bethesda, Maryland 20892.
Clin Immunol Immunopathol ; 52(3): 447-59, 1989 Sep.
Article em En | MEDLINE | ID: mdl-2547539
ABSTRACT
The role of interleukin-2 (IL-2) in the activation of suppressor T cells was investigated using the monoclonal antibody anti-Tac, which blocks the binding of IL-2 to the 55-kDa IL-2-binding peptide. The addition of anti-Tac during a preculture period inhibited the generation of Epstein-Barr virus (EBV)-induced suppressor T cells and of suppressor T cells induced in an antigen-specific system by a high antigen (sheep red blood cell) concentration. The cells activated by a short 2- or 7-day preculture period with EBV to become suppressor effectors were of the T8, Tac-positive phenotype. However, the T8-positive T cells obtained from peripheral blood mononuclear cells precultured with EBV for 14 days continued to manifest suppressor function, even though they were no longer Tac positive. In summary, our studies indicate that anti-Tac, by producing a functional blockade of human IL-2 receptors, inhibits the generation of suppressor T cells in antigen-specific as well as antigen-nonspecific systems and that cells that no longer express the Tac antigen may also function as suppressors.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Ativação Linfocitária / Receptores de Interleucina-2 / Interleucina-2 / Linfócitos T Reguladores Limite: Humans Idioma: En Revista: Clin Immunol Immunopathol Ano de publicação: 1989 Tipo de documento: Article
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Ativação Linfocitária / Receptores de Interleucina-2 / Interleucina-2 / Linfócitos T Reguladores Limite: Humans Idioma: En Revista: Clin Immunol Immunopathol Ano de publicação: 1989 Tipo de documento: Article
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