Chemmannur , S.V. and Badhwar , A.J. and Mirlekar, B. and Malonia , S.K. and Gupta, M. and Wadhwa , N. and Bopanna, R. and Mabalirajan , U. and Majumdar , S. and Ghosh , B. and Chattopadhyay , S. and UNSPECIFIED (2015) Nuclear matrix binding protein SMAR1 regulates T-cell differentiation and allergic airway disease. MucosalImmunology. pp. 1-11.

Text 22. Dr. Samit (Mucosal Immu) Open Access.pdf - Published Version Restricted to Repository staff only Download (531Kb) | Request a copy

Abstract

Asthma is a complex airway allergic disease involving the interplay of various cell types, cytokines, and transcriptional factors. Though many factors contribute to disease etiology, the molecular control of disease phenotype and responsiveness is not well understood. Here we report an essential role of the matrix attachment region (MAR)-binding protein SMAR1 in regulating immune response during allergic airway disease. Conditional knockout of SMAR1 in T cells rendered the mice resistant to eosinophilic airway inflammation against ovalbumin (OVA) allergen with low immunoglobulin E (IgE) and interleukin-5 (IL-5) levels. Moreover, a lower IgE/IgG2a ratio and higher interferon-c (IFN-c) response suggested aberrant skewing of T-cell differentiation toward type 1 helper Tcell (Th1) response. We show that SMAR1 functions as a negative regulator of Th1 and Th17 differentiation by interacting with two potential and similar MARregions present on the promoters of T-bet and IL-17. Thus, wepresentSMAR1as a regulator of T-cell differentiation that favors the establishment of Th2 cells by modulating Th1 and Th17 responses.

Item Type:	Article
Additional Information:	This is Open Access Journal (for full text click above weblink)
Subjects:	Infection and Immunity
Depositing User:	Mr. Rameshwar Nema
Date Deposited:	29 Apr 2015 06:22
Last Modified:	18 Dec 2021 13:29
URI:	http://nccs.sciencecentral.in/id/eprint/166

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