Abstract
Interleukin-10 (IL-10) plays an important immunopathogenic role in immunologic diseases, especially in HIV infection and atopic dermatitis. The control and regulatory mechanisms of IL-10 production have not been described in these diseases. Recently, we demonstrated that HIV-1 Nef induces IL-10 production in monocytes and that staphylococcal enterotoxin A (SEA) induces IL-10 production in T-lymphocytes. Here we show that Nef-induced IL-10 production and mRNA expression are strongly blocked by rapamycin, but are not blocked by cyclosporin (CsA) or FK506. Conversely, we show that CsA and FK506 completely inhibit SEA-induced IL-10 protein production and mRNA expression. The results of this study demonstrate that IL-10 production by Nef and SEA is controlled and regulated by different mechanisms.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Cells, Cultured
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Cyclosporine / pharmacology
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Enterotoxins / immunology*
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Enterotoxins / pharmacology
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Enzyme-Linked Immunosorbent Assay
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Gene Products, nef / immunology*
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Gene Products, nef / pharmacology
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HIV-1 / immunology*
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Humans
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Immunosuppressive Agents / pharmacology
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Interleukin-10 / genetics
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Interleukin-10 / metabolism*
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Leukocytes, Mononuclear / drug effects*
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Leukocytes, Mononuclear / immunology
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Leukocytes, Mononuclear / metabolism
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RNA, Messenger / analysis
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RNA, Messenger / drug effects
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Reverse Transcriptase Polymerase Chain Reaction
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Sirolimus / pharmacology
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Tacrolimus / pharmacology
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nef Gene Products, Human Immunodeficiency Virus
Substances
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Enterotoxins
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Gene Products, nef
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Immunosuppressive Agents
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RNA, Messenger
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nef Gene Products, Human Immunodeficiency Virus
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Interleukin-10
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enterotoxin A, Staphylococcal
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Cyclosporine
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Sirolimus
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Tacrolimus