title: IL-2 upregulates CD86 expression on human CD4(+) and CD8(+) T cells.
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.
authors.affiliation: Institute for Transfusion Medicine, Hannover Medical School, D-30625 Hannover, Germany. paine.ananta@mh-hannover.de
authors.forename: Ananta
authors.initials: A
authors.lastname: Paine
authors.forename: Hartmut
authors.initials: H
authors.lastname: Kirchner
authors.forename: Stephan
authors.initials: S
authors.lastname: Immenschuh
authors.forename: Mathias
authors.initials: M
authors.lastname: Oelke
authors.forename: Rainer
authors.initials: R
authors.lastname: Blasczyk
authors.forename: Britta
authors.initials: B
authors.lastname: Eiz-Vesper
mesh_terms: D018122:B7-1 Antigen / Q000096:biosynthesis; D051940:B7-2 Antigen / Q000096:biosynthesis*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D002478:Cells, Cultured; D006801:Humans; D016898:Interferon-alpha / Q000378:metabolism; D007376:Interleukin-2 / Q000276:immunology / Q000378:metabolism*; D053645:Interleukin-2 Receptor alpha Subunit / Q000276:immunology; D008213:Lymphocyte Activation; D050778:NFATC Transcription Factors / Q000037:antagonists & inhibitors; D058570:TOR Serine-Threonine Kinases / Q000037:antagonists & inhibitors
chemical_list: D018122:B7-1 Antigen; D051940:B7-2 Antigen; D016898:Interferon-alpha; D007376:Interleukin-2; D053645:Interleukin-2 Receptor alpha Subunit; D050778:NFATC Transcription Factors; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases