IL-2 upregulates CD86 expression on human CD4 +and CD8 + T cells

Ananta Paine, Hartmut Kirchner, Stephan Immenschuh, Mathias Oelke, Rainer Blasczyk, Britta Eiz-Vesper

Research output: Contribution to journalArticle

Abstract

The glycoprotein CD86 is an important costimulatory molecule that has been shown to be predominantly expressed on APCs, such as dendritic cells, macrophages, and B cells. More recently, CD86 was also detected on T cells in specific pathological conditions. The mechanisms of how CD86 might be induced and its functional role in T cells are not well understood. In the present study, we showed that treatment with IL-2 markedly upregulated CD86, but not CD80, in human CD4 + and CD8 + T cells. This upregulation occurred in the absence of bystander cells, and isolated naive CD4 + or CD8 + T cells exhibited different time-dependent CD86-expression patterns in response to IL-2. Upregulation of CD86 on activated T cells was reduced by Abs that block IL-2 and IL-2Rα (CD25), indicating a receptor-mediated mechanism. IL-2-dependent CD86 upregulation was blocked by pharmacological inhibitors of the NFAT and mammalian target of rapamycin pathways and was largely reduced by simultaneous exposure to IFN-α. Importantly, a marked increase in CD86 on T cells was also observed in vivo in IL-2-treated patients. In conclusion, IL-2 upregulates CD86 expression on human CD4 + and CD8 + T cells via a receptor-dependent mechanism that involves the NFAT and mammalian target of rapamycin pathways.

Original languageEnglish (US)
Pages (from-to)1620-1629
Number of pages10
JournalJournal of Immunology
Volume188
Issue number4
DOIs
StatePublished - Feb 15 2012

ASJC Scopus subject areas

  • Immunology

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    Paine, A., Kirchner, H., Immenschuh, S., Oelke, M., Blasczyk, R., & Eiz-Vesper, B. (2012). IL-2 upregulates CD86 expression on human CD4 +and CD8 + T cells. Journal of Immunology, 188(4), 1620-1629. https://doi.org/10.4049/jimmunol.1100181