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- W4313374440 abstract "Abstract Interleukin (IL)-17A is an important cytokine associated with autoimmune diseases and host defense. The mechanism of its action depends upon its ability to induce pro-inflammatory cytokines, e.g., IL-6, IL-8 as well as anti-fungal genes, e.g., b-defensin, CCL-20, CXCL-1. Most non-hematopoietic cells express IL-17 receptors and respond to IL-17A. Several regulators of each of the two independent arms of IL-17A signaling- gene induction and mRNA stabilization of inflammatory genes, are known; however, there is limited knowledge of how two arms influence each other. We previously reported the increased presence of 14-3-3 proteins in the inflamed aortic tissue, an autoimmune disease with increased IL-17A levels. This study led us to investigate the role of 14-3-3zeta(z) in the IL-17A signaling. By genetic manipulations in human and mouse cells, we observed that 14-3-3z is required for the IL-17A-induced IL-6 production by fibroblast and epithelial cells. Contrary to IL-6, 14-3-3z suppressed the CXCL-1 production in response to IL-17A. In the absence of 14-3-3z, IL-17A induction of anti-fungal genes (b-defensin) was completely suppressed. The mechanism of 14-3-3z action depends upon its interaction with Traf/Act1/IL-17R signaling. Our results show that 14-3-3z is an essential component of IL-17A signaling and its interaction with receptor complex provides a new model of regulating the output in IL-17A effector cells. To the best of our knowledge, this is the first report of the 14-3-3z role in regulating IL-17A induced outputs." @default.
- W4313374440 created "2023-01-06" @default.
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- W4313374440 date "2020-05-01" @default.
- W4313374440 modified "2023-09-27" @default.
- W4313374440 title "Novel Mechanism of Regulating IL-17 Signaling by 14-3-3zeta" @default.
- W4313374440 doi "https://doi.org/10.4049/jimmunol.204.supp.79.16" @default.
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