{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He M"],"funding":["NIBIB NIH HHS","NIAID NIH HHS","NCI NIH HHS","NIAMS NIH HHS"],"pagination":["eabg2752"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10424698"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["379(6633)"],"pubmed_abstract":["The induction of proinflammatory T cells by dendritic cell (DC) subtypes is critical for antitumor responses and effective immune checkpoint blockade (ICB) therapy. Here, we show that human CD1c<sup>+</sup>CD5<sup>+</sup> DCs are reduced in melanoma-affected lymph nodes, with CD5 expression on DCs correlating with patient survival. Activating CD5 on DCs enhanced T cell priming and improved survival after ICB therapy. CD5<sup>+</sup> DC numbers increased during ICB therapy, and low interleukin-6 (IL-6) concentrations promoted their de novo differentiation. Mechanistically, CD5 expression by DCs was required to generate optimally protective CD5<sup>hi</sup> T helper and CD8<sup>+</sup> T cells; further, deletion of CD5 from T cells dampened tumor elimination in response to ICB therapy in viv"],"journal":["Science (New York, N.Y.)"],"pubmed_title":["CD5 expression by dendritic cells directs T cell immunity and sustains immunotherapy responses."],"pmcid":["PMC10424698"],"funding_grant_id":["R01 AI022553","P50 AR080594","R01 AI166313","T32 CA009547","P30 CA091842","R01 AR075959","P30 CA016042","R01 AR073252","R01 AR040312","R01 CA245277","R21 EB024767","R01 AR074302"],"pubmed_authors":["White M","Pellegrini M","Sette A","Donermeyer D","Klechevsky E","Gubin MM","Schutt C","Garin V","Zhao Y","Shah K","Bak R","Korenfeld D","Ferris S","Schreiber RD","Ulezko Antonova A","Lindestam Arlehamn C","Gorvel L","Jensen TI","Modlin RL","He M","Allen PM","Roussak K","Fields RC","Gray J","Borcherding N","Luo J","Tung T","Bhatia H","Iberg CA","Dinkel S","Ma F"],"additional_accession":[]},"is_claimable":false,"name":"CD5 expression by dendritic cells directs T cell immunity and sustains immunotherapy responses.","description":"The induction of proinflammatory T cells by dendritic cell (DC) subtypes is critical for antitumor responses and effective immune checkpoint blockade (ICB) therapy. Here, we show that human CD1c<sup>+</sup>CD5<sup>+</sup> DCs are reduced in melanoma-affected lymph nodes, with CD5 expression on DCs correlating with patient survival. Activating CD5 on DCs enhanced T cell priming and improved survival after ICB therapy. CD5<sup>+</sup> DC numbers increased during ICB therapy, and low interleukin-6 (IL-6) concentrations promoted their de novo differentiation. Mechanistically, CD5 expression by DCs was required to generate optimally protective CD5<sup>hi</sup> T helper and CD8<sup>+</sup> T cells; further, deletion of CD5 from T cells dampened tumor elimination in response to ICB therapy in viv","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2026-05-28T18:44:15.46Z","creation":"2025-04-06T22:00:31.869Z"},"accession":"S-EPMC10424698","cross_references":{"pubmed":["36795805"],"doi":["10.1126/science.abg2752"]}}