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Interleukin-2 inhibition of oligodendrocyte progenitor cell proliferation depends on expression of the TAC receptor.
Saneto, R P; Chiappelli, F; de Vellis, J.
Afiliación
  • Saneto RP; Department of Anatomy, UCLA School of Medicine.
J Neurosci Res ; 18(1): 147-54, 1987.
Article en En | MEDLINE | ID: mdl-3500322
Interleukin-2 (IL-2) has been shown to inhibit oligodendrocyte progenitor cell proliferation. Within the immune system, IL-2 biological action is dependent strictly on the expression of the IL-2 receptor. The antibody TAC, which specifically binds the lymphocyte IL-2 receptor, has been shown to also bind oligodendrocyte progenitor cells cultured in a serumless, chemically defined medium. The expression of the TAC antigen was found necessary for IL-2 inhibition of oligodendrocyte progenitor cell proliferation. After IL-2 induced down-regulation of the TAC antigen, the progenitor cell was unresponsive to IL-2, even 72 hr after IL-2 withdrawal. During this unresponsive period, the oligodendrocyte progenitor cell was immunocytochemically negative for the TAC antigen. Thus, in contrast to IL-2 receptors on T-cells, IL-2 does not up-regulate its receptor on oligodendrocyte progenitor cells. However, upon interleukin 1 (IL-1) addition both IL-2 responsiveness and TAC immunocytochemical staining reappeared. These data suggest that IL-2 inhibition of progenitor cell proliferation depends on the expression of the TAC antigen, which can be regulated by IL-1.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores de Antígenos de Linfocitos T / Receptores Inmunológicos / Oligodendroglía / Neuroglía / Interleucina-2 Límite: Animals Idioma: En Revista: J Neurosci Res Año: 1987 Tipo del documento: Article Pais de publicación: Estados Unidos
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores de Antígenos de Linfocitos T / Receptores Inmunológicos / Oligodendroglía / Neuroglía / Interleucina-2 Límite: Animals Idioma: En Revista: J Neurosci Res Año: 1987 Tipo del documento: Article Pais de publicación: Estados Unidos