{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Schutt SD"],"funding":["NIAID NIH HHS","National Institutes of Health, National Institute of Allergy and Infectious Diseases, National Institute of Allergy and Infectious Diseases"],"pagination":["e143950"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9621143"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["132(21)"],"pubmed_abstract":["Graft-versus-host disease (GVHD), manifesting as either acute (aGVHD) or chronic (cGVHD), presents significant life-threatening complications following allogeneic hematopoietic cell transplantation. Here, we investigated Friend virus leukemia integration 1 (Fli-1) in GVHD pathogenesis and validated Fli-1 as a therapeutic target. Using genetic approaches, we found that Fli-1 dynamically regulated different T cell subsets in allogeneic responses and pathogenicity in the development of aGVHD and cGVHD. Compared with homozygous Fli1-deficient or WT T cells, heterozygous Fli1-deficient T cells induced the mildest GVHD, as evidenced by the lowest Th1 and Th17 cell differentiation. Single-cell RNA-Seq analysis revealed that Fli-1 differentially regulated CD4+ and CD8+ T cell responses. Fli-1 prom"],"journal":["The Journal of clinical investigation"],"pubmed_title":["The druggable transcription factor Fli-1 regulates T cell immunity and tolerance in graft-versus-host disease."],"pmcid":["PMC9621143"],"funding_grant_id":["R01 Al118305,R01 HL140953","R01 AI148403"],"pubmed_authors":["Ben-David Y","Mealer C","McDaniel Mims B","Choi HJ","Cui W","Kharel A","Helke K","Hanief Sofi M","Bastian D","Nguyen H","Zhang X","Liu C","Yu XZ","Wu Y","Schutt SD"],"additional_accession":[]},"is_claimable":false,"name":"The druggable transcription factor Fli-1 regulates T cell immunity and tolerance in graft-versus-host disease.","description":"Graft-versus-host disease (GVHD), manifesting as either acute (aGVHD) or chronic (cGVHD), presents significant life-threatening complications following allogeneic hematopoietic cell transplantation. Here, we investigated Friend virus leukemia integration 1 (Fli-1) in GVHD pathogenesis and validated Fli-1 as a therapeutic target. Using genetic approaches, we found that Fli-1 dynamically regulated different T cell subsets in allogeneic responses and pathogenicity in the development of aGVHD and cGVHD. Compared with homozygous Fli1-deficient or WT T cells, heterozygous Fli1-deficient T cells induced the mildest GVHD, as evidenced by the lowest Th1 and Th17 cell differentiation. Single-cell RNA-Seq analysis revealed that Fli-1 differentially regulated CD4+ and CD8+ T cell responses. Fli-1 prom","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Nov","modification":"2025-04-26T20:46:47.989Z","creation":"2025-04-06T16:31:56.78Z"},"accession":"S-EPMC9621143","cross_references":{"pubmed":["36074578"],"doi":["10.1172/JCI143950"]}}