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• W2064918219 abstract "Background. FK506 perturbs normal phosphorylation by inhibition of the PP2B protein phosphatase, calcineurin.Calcineurin activity is required for intracellular signal transduction via the T cell receptor that in turn leads to either TH1, or TH2, -type responses to antigen. This choice of response involves differential phosphorylation of STATS (S ignal T ransducers and A ctivators of T ranscription) for induction of STAT activity. Interferon-γ activates STAT1, a TH1-type mediator, and interleukin-4 activates STAT6, a TH2-type mediator. We ask if FK506 biases STAT activation toward a TH2-type response. Methods. Cells of the RAW 264.7 mouse macrophage line were treated with interleukin-4, or interferon-γ, plus or minus FK506, and any effect on STAT6 and STAT1 was compared. Results. Interleukin-4 specifically induced activation of STAT6, and pretreatment with FK506 enhanced this activity. Interferon-γ induced STAT1 activity but this was not influenced by FK506 pretreatment . Conclusion. FK506 protects against allograft rejection by inhibiting interleukin-2 production. Such protection may be enhanced by FK506-mediated up-regulation of STAT6 activity." @default.
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• W2064918219 date "2000-04-01" @default.
• W2064918219 modified "2023-09-24" @default.
• W2064918219 title "STAT 6 UP-REGULATION BY FK506 IN THE PRESENCE OF INTERLEUKIN-4" @default.
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• W2064918219 doi "https://doi.org/10.1097/00007890-200004150-00056" @default.
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