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CD40 activation boosts T cell immunity in vivo by enhancing T cell clonal expansion and delaying peripheral T cell deletion.
Maxwell, J R; Campbell, J D; Kim, C H; Vella, A T.
Afiliación
  • Maxwell JR; Department of Microbiology, Oregon State University, Corvallis 97331, USA.
J Immunol ; 162(4): 2024-34, 1999 Feb 15.
Article en En | MEDLINE | ID: mdl-9973474
In this report we show that activation of APC with an agonist anti-CD40 mAb profoundly alters the behavior of CD4 T cells in vivo. Stimulation of mice with anti-CD40 2 days before, but not 1 day after, administration of superantigen (SAg) enhanced CD4 and CD8 T cell clonal expansion by approximately threefold. Further, CD40 activation also delayed peripheral T cell deletion after activation. Dying, activated T cells were quantitated by detecting extracellular phosphatidylserine with concomitant staining for SAg-reactive T cells using a TCR Vbeta-specific mAb. Upon close examination, it was shown that CD40 activation delayed the death of the activated T cells. Additionally, it was found that enhanced survival of CD4 T cells was equally dependent on APC expression of B7-1 and B7-2. This is in contrast to CD8 T cells, which did not depend as much on B7-1 as B7-2. Thus, CD40 activation indirectly promotes T cell growth and delays the death of SAg-stimulated CD4 T cells in vivo. These data suggest that one way CD40 activation promotes a more robust immune response is by indirectly increasing the production of effector T cells and by keeping them alive for longer periods of time.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos T / Supresión Clonal / Antígenos CD40 Límite: Animals Idioma: En Revista: J Immunol Año: 1999 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos T / Supresión Clonal / Antígenos CD40 Límite: Animals Idioma: En Revista: J Immunol Año: 1999 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos