Nuclear matrix binding protein SMAR1 regulates T-cell differentiation and allergic airway disease

Mucosal Immunology
S V ChemmannurS Chattopadhyay

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-γ (IFN-γ) response suggested aberrant skewing of T-cell differentiation toward type 1 helper T cell (Th1) response. We show that SMAR1 functions as a negative regulator of Th1 and Th17 differentiation by interacting with two potential and similar MAR regions present on the promoters of T-bet and IL-17. Thus, we present SMAR1 as a regulator of T-cell differentiation that favors the establishment of Th2 cells by modulating Th1 and Th17 responses.

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Citations

Dec 22, 2017·PLoS Pathogens·Simon P JochemsDaniela M Ferreira
Feb 25, 2017·Frontiers in Immunology·Bhalchandra MirlekarSamit Chattopadhyay
Jul 3, 2019·Nucleic Acids Research·Nitin NarwadeAbhijeet Kulkarni
Apr 20, 2016·Nature Immunology·Reinhard Hinterleitner, Bana Jabri
Aug 28, 2021·Biochimica Et Biophysica Acta. Molecular and Cell Biology of Lipids·Richa PantSamit Chattopadhyay

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Methods Mentioned

BETA
PCR
imaging techniques
transfection
immunoprecipitation
ChIP
acetylation
bronchoalveolar
lavage
protein assay
enzyme-linked immunosorbant assay

Software Mentioned

Graph Pad Prism
FACS DIVA

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