<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chowdhury RR</submitter><funding>Howard Hughes Medical Institute</funding><funding>NIA NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>1510-1530</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9286288</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>130(10)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Coronary artery disease is an incurable, life-threatening disease that was once considered primarily a disorder of lipid deposition. Coronary artery disease is now also characterized by chronic inflammation' notable for the buildup of atherosclerotic plaques containing immune cells in various states of activation and differentiation. Understanding how these immune cells contribute to disease progression may lead to the development of novel therapeutic strategies.&lt;h4>Methods&lt;/h4>We used single-cell technology and in vitro assays to interrogate the immune microenvironment of human coronary atherosclerotic plaque at different stages of maturity.&lt;h4>Results&lt;/h4>In addition to macrophages, we found a high proportion of αβ T cells in the coronary plaques. Most of these T cells</pubmed_abstract><journal>Circulation research</journal><pubmed_title>Human Coronary Plaque T Cells Are Clonal and Cross-React to Virus and Self.</pubmed_title><pmcid>PMC9286288</pmcid><funding_grant_id>DP2 HL157540</funding_grant_id><funding_grant_id>R01 HL134830</funding_grant_id><funding_grant_id>F32 HL143847</funding_grant_id><funding_grant_id>P01 AI153559</funding_grant_id><funding_grant_id>R03 AG060182</funding_grant_id><funding_grant_id>T32 AI007290</funding_grant_id><pubmed_authors>Quertermous T</pubmed_authors><pubmed_authors>Tso A</pubmed_authors><pubmed_authors>Chien YH</pubmed_authors><pubmed_authors>Gulati GS</pubmed_authors><pubmed_authors>Ahmad H</pubmed_authors><pubmed_authors>Lee AS</pubmed_authors><pubmed_authors>Bakerman I</pubmed_authors><pubmed_authors>Jensen A</pubmed_authors><pubmed_authors>Sokol J</pubmed_authors><pubmed_authors>Koyano T</pubmed_authors><pubmed_authors>Gopakumar J</pubmed_authors><pubmed_authors>Liang G</pubmed_authors><pubmed_authors>Cheng P</pubmed_authors><pubmed_authors>Fong R</pubmed_authors><pubmed_authors>Boyd J</pubmed_authors><pubmed_authors>Davis MM</pubmed_authors><pubmed_authors>D'Addabbo J</pubmed_authors><pubmed_authors>Louis DM</pubmed_authors><pubmed_authors>Shankar V</pubmed_authors><pubmed_authors>Nguyen PK</pubmed_authors><pubmed_authors>Woo YJ</pubmed_authors><pubmed_authors>Chowdhury RR</pubmed_authors><pubmed_authors>Chan CKF</pubmed_authors><pubmed_authors>Wirka R</pubmed_authors><pubmed_authors>Wendel BS</pubmed_authors><pubmed_authors>Nau AN</pubmed_authors><pubmed_authors>Veizades S</pubmed_authors><pubmed_authors>Jaiswal S</pubmed_authors><pubmed_authors>Huang X</pubmed_authors><pubmed_authors>Sasagawa K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Human Coronary Plaque T Cells Are Clonal and Cross-React to Virus and Self.</name><description>&lt;h4>Background&lt;/h4>Coronary artery disease is an incurable, life-threatening disease that was once considered primarily a disorder of lipid deposition. Coronary artery disease is now also characterized by chronic inflammation' notable for the buildup of atherosclerotic plaques containing immune cells in various states of activation and differentiation. Understanding how these immune cells contribute to disease progression may lead to the development of novel therapeutic strategies.&lt;h4>Methods&lt;/h4>We used single-cell technology and in vitro assays to interrogate the immune microenvironment of human coronary atherosclerotic plaque at different stages of maturity.&lt;h4>Results&lt;/h4>In addition to macrophages, we found a high proportion of αβ T cells in the coronary plaques. Most of these T cells</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 May</publication><modification>2026-05-28T06:15:19.402Z</modification><creation>2024-11-12T18:05:33.869Z</creation></dates><accession>S-EPMC9286288</accession><cross_references><pubmed>35430876</pubmed><doi>10.1161/circresaha.121.320090</doi><doi>10.1161/CIRCRESAHA.121.320090</doi></cross_references></HashMap>