{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wedel J"],"funding":["NIH NIAID","Isabella Julian Forrest Foundation","Casey Lee Ball Foundation"],"pagination":["e172218"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12208552"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["135(13)"],"pubmed_abstract":["Coinhibitory receptors function as central modulators of the immune response to resolve T effector activation and/or to sustain immune homeostasis. Here, using humanized SCID mice, we found that neuropilin-2 (NRP2) is inducible on late effector and exhausted subsets of human CD4+ T cells and that it is coexpressed with established coinhibitory molecules including PD-1, CTLA4, TIGIT, LAG3, and TIM3. In murine models, we also found that NRP2 is expressed on effector memory CD4+ T cells with an exhausted phenotype and that it functions as a key coinhibitory molecule. Knockout (KO) of NRP2 resulted in hyperactive CD4+ T cell responses and enhanced inflammation in delayed-type hypersensitivity and transplantation models. After cardiac transplantation, allograft rejection and graft failure were "],"journal":["The Journal of clinical investigation"],"pubmed_title":["Neuropilin-2 functions as a coinhibitory receptor to regulate antigen-induced inflammation and allograft rejection."],"pmcid":["PMC12208552"],"funding_grant_id":["N/A","R01AI148539"],"pubmed_authors":["Nakayama H","Briscoe DM","Bose S","Liu K","Zhang H","MacLeod K","Wedel J","Lee JW","Bielenberg DR","Kochupurakkal N","Maslyar M","Kong SW","Alsairafi B","Komatsu M"],"additional_accession":[]},"is_claimable":false,"name":"Neuropilin-2 functions as a coinhibitory receptor to regulate antigen-induced inflammation and allograft rejection.","description":"Coinhibitory receptors function as central modulators of the immune response to resolve T effector activation and/or to sustain immune homeostasis. Here, using humanized SCID mice, we found that neuropilin-2 (NRP2) is inducible on late effector and exhausted subsets of human CD4+ T cells and that it is coexpressed with established coinhibitory molecules including PD-1, CTLA4, TIGIT, LAG3, and TIM3. In murine models, we also found that NRP2 is expressed on effector memory CD4+ T cells with an exhausted phenotype and that it functions as a key coinhibitory molecule. Knockout (KO) of NRP2 resulted in hyperactive CD4+ T cell responses and enhanced inflammation in delayed-type hypersensitivity and transplantation models. After cardiac transplantation, allograft rejection and graft failure were ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jul","modification":"2026-06-01T15:31:49.139Z","creation":"2026-04-08T13:44:39.872Z"},"accession":"S-EPMC12208552","cross_references":{"pubmed":["40590224"],"doi":["10.1172/JCI172218"]}}