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http://purl.uniprot.org/citations/29221730http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29221730http://www.w3.org/2000/01/rdf-schema#comment"CD4+ T cells orchestrate immune responses and destruction of allogeneic organ transplants, but how this process is regulated on a transcriptional level remains unclear. Here, we demonstrated that interferon regulatory factor 4 (IRF4) was a key transcriptional determinant controlling T cell responses during transplantation. IRF4 deletion in mice resulted in progressive establishment of CD4+ T cell dysfunction and long-term allograft survival. Mechanistically, IRF4 repressed PD-1, Helios, and other molecules associated with T cell dysfunction. In the absence of IRF4, chromatin accessibility and binding of Helios at PD-1 cis-regulatory elements were increased, resulting in enhanced PD-1 expression and CD4+ T cell dysfunction. The dysfunctional state of Irf4-deficient T cells was initially reversible by PD-1 ligand blockade, but it progressively developed into an irreversible state. Hence, IRF4 controls a core regulatory circuit of CD4+ T cell dysfunction, and targeting IRF4 represents a potential therapeutic strategy for achieving transplant acceptance."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.org/dc/terms/identifier"doi:10.1016/j.immuni.2017.11.003"xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Chen W."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Fan Y."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Shi X."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Wu J."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Xiao X."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Xia J."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Li X.C."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Minze L.J."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Sciammas R."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/author"Ghobrial R.M."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/name"Immunity"xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/pages"1114-1128.e6"xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/title"Ablation of Transcription Factor IRF4 Promotes Transplant Acceptance by Driving Allogenic CD4+ T Cell Dysfunction."xsd:string
http://purl.uniprot.org/citations/29221730http://purl.uniprot.org/core/volume"47"xsd:string
http://purl.uniprot.org/citations/29221730http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29221730
http://purl.uniprot.org/citations/29221730http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29221730
http://purl.uniprot.org/uniprot/#_A0A3Q4EC35-mappedCitation-29221730http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29221730
http://purl.uniprot.org/uniprot/#_A0A3Q4EC46-mappedCitation-29221730http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29221730
http://purl.uniprot.org/uniprot/#_A0A1Y7VIT1-mappedCitation-29221730http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29221730