<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cook KD</submitter><funding>North Carolina Translational and Clinical Sciences Institute, University of North Carolina at Chapel Hill</funding><funding>University of North Carolina</funding><funding>NIAID NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIGMS NIH HHS</funding><pagination>703-14</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4731234</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>43(4)</volume><pubmed_abstract>Epigenetic changes, including histone methylation, control T cell differentiation and memory formation, though the enzymes that mediate these processes are not clear. We show that UTX, a histone H3 lysine 27 (H3K27) demethylase, supports T follicular helper (Tfh) cell responses that are essential for B cell antibody generation and the resolution of chronic viral infections. Mice with a T cell-specific UTX deletion had fewer Tfh cells, reduced germinal center responses, lacked virus-specific immunoglobulin G (IgG), and were unable to resolve chronic lymphocytic choriomeningitis virus infections. UTX-deficient T cells showed decreased expression of interleukin-6 receptor-α and other Tfh cell-related genes that were associated with increased H3K27 methylation. Additionally, Turner Syndrome su</pubmed_abstract><journal>Immunity</journal><pubmed_title>T Follicular Helper Cell-Dependent Clearance of a Persistent Virus Infection Requires T Cell Expression of the Histone Demethylase UTX.</pubmed_title><pmcid>PMC4731234</pmcid><funding_grant_id>R56 AI110682</funding_grant_id><funding_grant_id>R01 NS079683</funding_grant_id><funding_grant_id>P30 CA016086</funding_grant_id><funding_grant_id>T32 AI007273</funding_grant_id><funding_grant_id>R01 GM101974</funding_grant_id><funding_grant_id>TTSA004P2</funding_grant_id><funding_grant_id>R01 GM10974</funding_grant_id><funding_grant_id>R01 AI074862</funding_grant_id><funding_grant_id>T32 AI7273-27</funding_grant_id><pubmed_authors>Whitfield-Larry F</pubmed_authors><pubmed_authors>Allard DE</pubmed_authors><pubmed_authors>Rager JE</pubmed_authors><pubmed_authors>Fry RC</pubmed_authors><pubmed_authors>Su MA</pubmed_authors><pubmed_authors>Magnuson T</pubmed_authors><pubmed_authors>Whitmire JK</pubmed_authors><pubmed_authors>Cook KD</pubmed_authors><pubmed_authors>Conley B</pubmed_authors><pubmed_authors>Shpargel KB</pubmed_authors><pubmed_authors>Starmer J</pubmed_authors><pubmed_authors>Davenport ML</pubmed_authors></additional><is_claimable>false</is_claimable><name>T Follicular Helper Cell-Dependent Clearance of a Persistent Virus Infection Requires T Cell Expression of the Histone Demethylase UTX.</name><description>Epigenetic changes, including histone methylation, control T cell differentiation and memory formation, though the enzymes that mediate these processes are not clear. We show that UTX, a histone H3 lysine 27 (H3K27) demethylase, supports T follicular helper (Tfh) cell responses that are essential for B cell antibody generation and the resolution of chronic viral infections. Mice with a T cell-specific UTX deletion had fewer Tfh cells, reduced germinal center responses, lacked virus-specific immunoglobulin G (IgG), and were unable to resolve chronic lymphocytic choriomeningitis virus infections. UTX-deficient T cells showed decreased expression of interleukin-6 receptor-α and other Tfh cell-related genes that were associated with increased H3K27 methylation. Additionally, Turner Syndrome su</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Oct</publication><modification>2025-04-04T01:17:40.696Z</modification><creation>2019-03-27T02:07:47Z</creation></dates><accession>S-EPMC4731234</accession><cross_references><pubmed>26431949</pubmed><doi>10.1016/j.immuni.2015.09.002</doi></cross_references></HashMap>