Suppression of Th17 cell differentiation by misshapen/NIK-related kinase MINK1

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Suppression of Th17 cell differentiation by misshapen/NIK-related kinase MINK1

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Title: Suppression of Th17 cell differentiation by misshapen/NIK-related kinase MINK1
Author: Fu, Guotong; Xu, Qin; Qiu, Yuanjun; Jin, Xuexiao; Xu, Ting; Dong, Shunli; Wang, Jianli; Ke, Yuehai; Hu, Hu; Cao, Xuetao; Wang, Di; Cantor, Harvey; Gao, Xiang; Lu, Linrong

Note: Order does not necessarily reflect citation order of authors.

Citation: Fu, G., Q. Xu, Y. Qiu, X. Jin, T. Xu, S. Dong, J. Wang, et al. 2017. “Suppression of Th17 cell differentiation by misshapen/NIK-related kinase MINK1.” The Journal of Experimental Medicine 214 (5): 1453-1469. doi:10.1084/jem.20161120. http://dx.doi.org/10.1084/jem.20161120.
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Abstract: T helper type 17 cells (Th17 cells) are major contributors to many autoimmune diseases. In this study, we demonstrate that the germinal center kinase family member MINK1 (misshapen/NIK-related kinase 1) negatively regulates Th17 cell differentiation. The suppressive effect of MINK1 on induction of Th17 cells is mediated by the inhibition of SMAD2 activation through direct phosphorylation of SMAD2 at the T324 residue. The importance of MINK1 to Th17 cell differentiation was strengthened in the animal model of experimental autoimmune encephalomyelitis (EAE). Moreover, we show that the reactive oxygen species (ROS) scavenger N-acetyl cysteine boosts Th17 cell differentiation in a MINK1-dependent manner and exacerbates the severity of EAE. Thus, we have not only established MINK1 as a critical regulator of Th17 cell differentiation, but also clarified that accumulation of ROS may limit the generation of Th17 cells. The contribution of MINK1 to ROS-regulated Th17 cell differentiation may suggest an important mechanism for the development of autoimmune diseases influenced by antioxidant dietary supplements.
Published Version: doi:10.1084/jem.20161120
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5413330/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:34493218
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