2015
Biochem Biophys Res Commun. 2015 Aug 21;464(2):647-53. doi: 10.1016/j.bbrc.2015.07.028. Epub 2015 Jul 10.
MAR binding protein SMAR1 favors IL-10 mediated regulatory T cell function in acute colitis.
Chromatin and Disease Biology Laboratory, National Centre for Cell Science, Ganeshkhind, Pune 411007, India. Experimental Animal Facility, National Centre for Cell Science, Ganeshkhind, Pune 411007, India.
Service type: Knockout mice
Abstract
Treg cells are not only crucial for controlling immune responses to autoantigens but also prevent those directed towards commensal pathogens. Control of effector immune responses by Treg cells depend on their capacity to accumulate at inflammatory site and accordingly accommodate to inflammatory environment. Till date, the factors associated with maintaining these aspects of Treg phenotype is not understood properly. Here we have shown that a known nuclear matrix binding protein SMAR1 is selectively expressed more in colonic Treg cells and is required for their ability to accumulate at inflammatory site and to sustain high levels of Foxp3 and IL-10 expression during acute colitis. Elimination of anti-inflammatory subsets revealed a protective role for IL-10 producing Treg cells in SMAR1(-/-) mice. Moreover, a combined action of Foxp3 and SMAR1 restricts effector cytokine production and enhance the production of IL-10 by colonic Treg cells that controls acute colitis. This data highlights a critical role of SMAR1 in maintaining Treg physiology during inflammatory disorders.
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