{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Laurie SJ"],"funding":["U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)","U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences","U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS)","NIDDK NIH HHS","NIEHS NIH HHS","NIAID NIH HHS","U.S. Department of Health & Human Services | NIH | National Cancer Institute","NHLBI NIH HHS","U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute","NCI NIH HHS","U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI)","NIGMS NIH HHS"],"pagination":["6000"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11255294"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"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"],"journal":["Nature communications"],"pubmed_title":["Type II innate lymphoid cell plasticity contributes to impaired reconstitution after allogeneic hematopoietic stem cell transplantation."],"pmcid":["PMC11255294"],"funding_grant_id":["1K12GM000678-20","P30 AI050410","T32GM067553","R01GM138912","R01CA276663","1T32CA211056-01A1","P30 ES010126","R01 GM138912","T32 CA196589","K12 GM000678","P30 CA016086","R01 HL139730","T32 CA211056","1R01HL155098-01A1","R01 CA276663","P30 DK034987","T32 GM067553","R01 HL155098","1R01HL139730-03"],"pubmed_authors":["Bruce DW","Laurie SJ","Foster JP","Parker JS","Bommiasamy H","Chao NJ","Davis IJ","Serody JS","Sarantopoulos S","Yazdimamaghani M","Kolupaev OV","Pattenden SG"],"additional_accession":[]},"is_claimable":false,"name":"Type II innate lymphoid cell plasticity contributes to impaired reconstitution after allogeneic hematopoietic stem cell transplantation.","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","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-06-02T22:56:27.267Z","creation":"2025-04-06T17:11:05.986Z"},"accession":"S-EPMC11255294","cross_references":{"pubmed":["39019846"],"doi":["10.1038/s41467-024-50263-7"]}}