MAR binding protein SMAR1 favors IL-10 mediated regulatory T cell function in acute colitis

Bhalchandra Mirlekar; Sachin Patil; Ramanamurthy Bopanna; Samit Chattopadhyay

doi:10.1016/j.bbrc.2015.07.028

MAR binding protein SMAR1 favors IL-10 mediated regulatory T cell function in acute colitis

Biochem Biophys Res Commun. 2015 Aug 21;464(2):647-53. doi: 10.1016/j.bbrc.2015.07.028. Epub 2015 Jul 10.

Authors

Bhalchandra Mirlekar¹, Sachin Patil¹, Ramanamurthy Bopanna², Samit Chattopadhyay³

Affiliations

¹ Chromatin and Disease Biology Laboratory, National Centre for Cell Science, Ganeshkhind, Pune 411007, India.
² Experimental Animal Facility, National Centre for Cell Science, Ganeshkhind, Pune 411007, India.
³ Chromatin and Disease Biology Laboratory, National Centre for Cell Science, Ganeshkhind, Pune 411007, India. Electronic address: samit@nccs.res.in.

PMID: 26168735
DOI: 10.1016/j.bbrc.2015.07.028

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.

Keywords: Colitis; DSS; IL-10; IL-17; SMAR1; T(reg).

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Acute Disease
Animals
Cell Cycle Proteins / genetics
Cell Cycle Proteins / physiology*
Cell Differentiation
Colitis / immunology*
DNA-Binding Proteins / genetics
DNA-Binding Proteins / physiology*
Interleukin-10 / physiology*
Mice
Mice, Knockout
Nuclear Proteins / genetics
Nuclear Proteins / physiology*
T-Lymphocytes, Regulatory / immunology*
T-Lymphocytes, Regulatory / pathology

Substances

Banp protein, mouse
Cell Cycle Proteins
DNA-Binding Proteins
Nuclear Proteins
Interleukin-10