<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Laurie SJ</submitter><funding>U.S. Department of Health &amp; Human Services | NIH | National Cancer Institute (NCI)</funding><funding>U.S. Department of Health &amp;amp; Human Services | NIH | National Institute of General Medical Sciences</funding><funding>U.S. Department of Health &amp; Human Services | NIH | National Institute of General Medical Sciences (NIGMS)</funding><funding>NIDDK NIH HHS</funding><funding>NIEHS NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>U.S. Department of Health &amp;amp; Human Services | NIH | National Cancer Institute</funding><funding>NHLBI NIH HHS</funding><funding>U.S. Department of Health &amp;amp; Human Services | NIH | National Heart, Lung, and Blood Institute</funding><funding>NCI NIH HHS</funding><funding>U.S. Department of Health &amp; Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI)</funding><funding>NIGMS NIH HHS</funding><pagination>6000</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11255294</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(1)</volume><pubmed_abstract>Type II innate lymphoid cells (ILC2s) maintain homeostasis and barrier integrity in mucosal tissues. In both mice and humans, ILC2s poorly reconstitute after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Determining the mechanisms involved in their impaired reconstitution could improve transplant outcomes. By integrating single-cell chromatin and transcriptomic analyses of transplanted ILC2s, we identify a previously unreported population of converted ILC1-like cells in the mouse small intestine post-transplant. Exposure of ILC2s to proinflammatory cytokines resulted in a mixed ILC1-ILC2 phenotype but was able to convert only a small population of ILC2s to ILC1s, which were found post-transplant. Whereas ILC2s protected against acute graft-versus-host disease (aGVHD) medi</pubmed_abstract><journal>Nature communications</journal><pubmed_title>Type II innate lymphoid cell plasticity contributes to impaired reconstitution after allogeneic hematopoietic stem cell transplantation.</pubmed_title><pmcid>PMC11255294</pmcid><funding_grant_id>1K12GM000678-20</funding_grant_id><funding_grant_id>P30 AI050410</funding_grant_id><funding_grant_id>T32GM067553</funding_grant_id><funding_grant_id>R01GM138912</funding_grant_id><funding_grant_id>R01CA276663</funding_grant_id><funding_grant_id>1T32CA211056-01A1</funding_grant_id><funding_grant_id>P30 ES010126</funding_grant_id><funding_grant_id>R01 GM138912</funding_grant_id><funding_grant_id>T32 CA196589</funding_grant_id><funding_grant_id>K12 GM000678</funding_grant_id><funding_grant_id>P30 CA016086</funding_grant_id><funding_grant_id>R01 HL139730</funding_grant_id><funding_grant_id>T32 CA211056</funding_grant_id><funding_grant_id>1R01HL155098-01A1</funding_grant_id><funding_grant_id>R01 CA276663</funding_grant_id><funding_grant_id>P30 DK034987</funding_grant_id><funding_grant_id>T32 GM067553</funding_grant_id><funding_grant_id>R01 HL155098</funding_grant_id><funding_grant_id>1R01HL139730-03</funding_grant_id><pubmed_authors>Bruce DW</pubmed_authors><pubmed_authors>Laurie SJ</pubmed_authors><pubmed_authors>Foster JP</pubmed_authors><pubmed_authors>Parker JS</pubmed_authors><pubmed_authors>Bommiasamy H</pubmed_authors><pubmed_authors>Chao NJ</pubmed_authors><pubmed_authors>Davis IJ</pubmed_authors><pubmed_authors>Serody JS</pubmed_authors><pubmed_authors>Sarantopoulos S</pubmed_authors><pubmed_authors>Yazdimamaghani M</pubmed_authors><pubmed_authors>Kolupaev OV</pubmed_authors><pubmed_authors>Pattenden SG</pubmed_authors></additional><is_claimable>false</is_claimable><name>Type II innate lymphoid cell plasticity contributes to impaired reconstitution after allogeneic hematopoietic stem cell transplantation.</name><description>Type II innate lymphoid cells (ILC2s) maintain homeostasis and barrier integrity in mucosal tissues. In both mice and humans, ILC2s poorly reconstitute after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Determining the mechanisms involved in their impaired reconstitution could improve transplant outcomes. By integrating single-cell chromatin and transcriptomic analyses of transplanted ILC2s, we identify a previously unreported population of converted ILC1-like cells in the mouse small intestine post-transplant. Exposure of ILC2s to proinflammatory cytokines resulted in a mixed ILC1-ILC2 phenotype but was able to convert only a small population of ILC2s to ILC1s, which were found post-transplant. Whereas ILC2s protected against acute graft-versus-host disease (aGVHD) medi</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2026-06-02T22:56:27.267Z</modification><creation>2025-04-06T17:11:05.986Z</creation></dates><accession>S-EPMC11255294</accession><cross_references><pubmed>39019846</pubmed><doi>10.1038/s41467-024-50263-7</doi></cross_references></HashMap>