<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hill DA</submitter><funding>NICHD NIH HHS</funding><funding>HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases</funding><funding>NIDDK NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>HHS | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development</funding><pagination>E5096-E5105</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5984532</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>115(22)</volume><pubmed_abstract>Obesity is characterized by an accumulation of macrophages in adipose, some of which form distinct crown-like structures (CLS) around fat cells. While multiple discrete adipose tissue macrophage (ATM) subsets are thought to exist, their respective effects on adipose tissue, and the transcriptional mechanisms that underlie the functional differences between ATM subsets, are not well understood. We report that obese fat tissue of mice and humans contain multiple distinct populations of ATMs with unique tissue distributions, transcriptomes, chromatin landscapes, and functions. Mouse Ly6c ATMs reside outside of CLS and are adipogenic, while CD9 ATMs reside within CLS, are lipid-laden, and are proinflammatory. Adoptive transfer of Ly6c ATMs into lean mice activates gene programs typical of norm</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Distinct macrophage populations direct inflammatory versus physiological changes in adipose tissue.</pubmed_title><pmcid>PMC5984532</pmcid><funding_grant_id>T32 HD043021</funding_grant_id><funding_grant_id>P30 MH097488</funding_grant_id><funding_grant_id>P30 DK019525</funding_grant_id><funding_grant_id>R01 DK049780</funding_grant_id><funding_grant_id>DK49780</funding_grant_id><funding_grant_id>R01 HL111501</funding_grant_id><funding_grant_id>F30 DK112507</funding_grant_id><pubmed_authors>Nelson VL</pubmed_authors><pubmed_authors>Kim J</pubmed_authors><pubmed_authors>Hill DA</pubmed_authors><pubmed_authors>Won KJ</pubmed_authors><pubmed_authors>Lazar MA</pubmed_authors><pubmed_authors>Kambayashi T</pubmed_authors><pubmed_authors>Ho WY</pubmed_authors><pubmed_authors>Lim HW</pubmed_authors><pubmed_authors>Kim YH</pubmed_authors><pubmed_authors>Nguyen HCB</pubmed_authors><pubmed_authors>Vallabhajosyula P</pubmed_authors><pubmed_authors>Chegireddy K</pubmed_authors><pubmed_authors>Habertheuer A</pubmed_authors><pubmed_authors>Foong YH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Distinct macrophage populations direct inflammatory versus physiological changes in adipose tissue.</name><description>Obesity is characterized by an accumulation of macrophages in adipose, some of which form distinct crown-like structures (CLS) around fat cells. While multiple discrete adipose tissue macrophage (ATM) subsets are thought to exist, their respective effects on adipose tissue, and the transcriptional mechanisms that underlie the functional differences between ATM subsets, are not well understood. We report that obese fat tissue of mice and humans contain multiple distinct populations of ATMs with unique tissue distributions, transcriptomes, chromatin landscapes, and functions. Mouse Ly6c ATMs reside outside of CLS and are adipogenic, while CD9 ATMs reside within CLS, are lipid-laden, and are proinflammatory. Adoptive transfer of Ly6c ATMs into lean mice activates gene programs typical of norm</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 May</publication><modification>2026-04-30T17:38:17.595Z</modification><creation>2019-03-27T00:09:29Z</creation></dates><accession>S-EPMC5984532</accession><cross_references><pubmed>29760084</pubmed><doi>10.1073/pnas.1802611115</doi></cross_references></HashMap>