Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/691
Full metadata record
DC FieldValueLanguage
dc.contributor.authorChattopadhyay, Samit-
dc.date.accessioned2016-03-22T09:49:07Z-
dc.date.available2016-03-22T09:49:07Z-
dc.date.issued2015-11-
dc.identifier.urihttp://hdl.handle.net/123456789/691-
dc.description.abstractAsthma 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.en_US
dc.publisherSociety for Mucosal Immunologyen_US
dc.titleNuclear matrix binding protein SMAR1 regulates T-cell differentiation and allergic airway diseaseen_US
dc.contributor.coauthorChemmannur, SV-
dc.contributor.coauthorBadhwar, AJ-
dc.contributor.coauthorMirlekar, B-
dc.contributor.coauthorMalonia, SK-
dc.contributor.coauthorGupta, M-
dc.contributor.coauthorWadhwa, N-
dc.contributor.coauthorBopanna, R-
dc.contributor.coauthorMabalirajan, U-
dc.contributor.coauthorMajumdar, Subeer S-
dc.contributor.coauthorGhosh, B-
dc.journalMucosal Immunologyen_US
dc.volumeno8en_US
dc.issueno6en_US
dc.pages1201-1211en_US
Appears in Collections:Cellular Endocrinology, Publications

Files in This Item:
File Description SizeFormat 
mi201511a.pdfResearch article2.3 MBAdobe PDFView/Open    Request a copy


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.