<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>6(2)</volume><submitter>Sasikala M</submitter><pubmed_abstract>&lt;h4>Objectives&lt;/h4>Altered immune homeostasis and involvement of T cells has been reported in chronic pancreatitis (CP). We evaluated the role of &lt;i>Bach2&lt;/i> (BTB and CNC homology basic leucine zipper transcription factor 2), a key regulator of immune homeostasis in the chronicity of CP.&lt;h4>Methods&lt;/h4>Expression of &lt;i>Bach2&lt;/i> and T-cell transcription factors, enumeration of BACH2+/CD4+ T-lymphocytes were performed by qRT-PCR and flow cytometry respectively. &lt;i>Bach2&lt;/i>silenced human CD4+ T-lymphocytes were exposed to CP tissue extract to assess T-cell lineage commitment. Aryl hydrocarbon receptor (&lt;i>Ahr&lt;/i>) and Deubiquitinase enzyme A (DUBA/&lt;i>OTUD5gene&lt;/i>) were evaluated as markers of persistent Th17 cell differentiation. &lt;i>Bach2&lt;/i> gene (exons) was sequenced to identify risk va</pubmed_abstract><journal>United European gastroenterology journal</journal><pagination>272-282</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5833222</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Bach2 repression mediates Th17 cell induced inflammation and associates with clinical features of advanced disease in chronic pancreatitis.</pubmed_title><pmcid>PMC5833222</pmcid><pubmed_authors>Murali Manohar K</pubmed_authors><pubmed_authors>Ghosh S</pubmed_authors><pubmed_authors>Aslam M</pubmed_authors><pubmed_authors>Pavan Kumar P</pubmed_authors><pubmed_authors>Pradeep R</pubmed_authors><pubmed_authors>Talukdar R</pubmed_authors><pubmed_authors>Reddy DN</pubmed_authors><pubmed_authors>Deshpande N</pubmed_authors><pubmed_authors>Rao GV</pubmed_authors><pubmed_authors>Ravikanth VV</pubmed_authors><pubmed_authors>Singh S</pubmed_authors><pubmed_authors>Sasikala M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Bach2 repression mediates Th17 cell induced inflammation and associates with clinical features of advanced disease in chronic pancreatitis.</name><description>&lt;h4>Objectives&lt;/h4>Altered immune homeostasis and involvement of T cells has been reported in chronic pancreatitis (CP). We evaluated the role of &lt;i>Bach2&lt;/i> (BTB and CNC homology basic leucine zipper transcription factor 2), a key regulator of immune homeostasis in the chronicity of CP.&lt;h4>Methods&lt;/h4>Expression of &lt;i>Bach2&lt;/i> and T-cell transcription factors, enumeration of BACH2+/CD4+ T-lymphocytes were performed by qRT-PCR and flow cytometry respectively. &lt;i>Bach2&lt;/i>silenced human CD4+ T-lymphocytes were exposed to CP tissue extract to assess T-cell lineage commitment. Aryl hydrocarbon receptor (&lt;i>Ahr&lt;/i>) and Deubiquitinase enzyme A (DUBA/&lt;i>OTUD5gene&lt;/i>) were evaluated as markers of persistent Th17 cell differentiation. &lt;i>Bach2&lt;/i> gene (exons) was sequenced to identify risk va</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Mar</publication><modification>2026-05-05T03:46:19.574Z</modification><creation>2026-04-07T21:22:01.961Z</creation></dates><accession>S-EPMC5833222</accession><cross_references><pubmed>29511557</pubmed><doi>10.1177/2050640617716596</doi></cross_references></HashMap>