{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T11:38:04Z","timestamp":1776425884939,"version":"3.51.2"},"reference-count":36,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2021,9,1]],"date-time":"2021-09-01T00:00:00Z","timestamp":1630454400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["RTG1949"],"award-info":[{"award-number":["RTG1949"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["RTG1949"],"award-info":[{"award-number":["RTG1949"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["RTG1949"],"award-info":[{"award-number":["RTG1949"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Neuropilin-1 (Nrp-1) is a well described marker molecule for CD4+Foxp3+ thymus-derived regulatory T cells (Tregs). In addition, a small population of CD4+Foxp3\u2212 conventional (conv) T cells expresses Nrp-1 in naive mice, and Nrp-1 expression has been described to be upregulated on activated CD4+ T cells. However, the function of Nrp-1 expression on CD4+ non-Tregs still remains elusive. In this study, we demonstrate that Nrp-1 expression was induced upon stimulation of CD4+Foxp3\u2212 T cells in vitro and during an ongoing immune response in vivo. This activation-induced Nrp-1+CD4+ T cell subset (iNrp-1+) showed a highly activated phenotype in terms of elevated CD25 and CD44 expression, enhanced production of proinflammatory cytokines, and increased proliferation compared with the Nrp-1\u2212CD4+ counterpart. In contrast, Nrp-1+CD4+Foxp3\u2212 conv T cells from naive mice (nNrp-1+) were dysfunctional. nNrp-1+CD4+ conv T cells upregulated activation-associated molecules to a lesser extent, exhibited impaired proliferation and produced fewer proinflammatory cytokines than Nrp-1\u2212CD4+ conv T cells upon stimulation in vitro. Moreover, the expression of PD-1 and CTLA-4 was significantly higher on nNrp-1+CD4+Foxp3\u2212 T cells compared with iNrp-1+CD4+Foxp3\u2212 T cells and Nrp-1\u2212CD4+Foxp3\u2212 T cells after stimulation and under homeostatic conditions. Strikingly, transfer of Ag-specific iNrp-1+CD4+ conv T cells aggravated diabetes development, whereas Ag-specific nNrp-1+CD4+ conv T cells failed to induce disease in a T cell transfer model of diabetes. Overall, our results indicate that Nrp-1 expression has opposite functions in recently activated CD4+ non-Tregs compared with CD4+ non-Tregs from naive mice.<\/jats:p>","DOI":"10.4049\/jimmunol.2100222","type":"journal-article","created":{"date-parts":[[2021,8,2]],"date-time":"2021-08-02T16:21:24Z","timestamp":1627921284000},"page":"1288-1297","source":"Crossref","is-referenced-by-count":7,"title":["Neuropilin-1 Is Expressed on Highly Activated CD4+ Effector T Cells and Dysfunctional CD4+ Conventional T Cells from Naive Mice"],"prefix":"10.1093","volume":"207","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8192-7761","authenticated-orcid":false,"given":"Hanna","family":"Abberger","sequence":"first","affiliation":[{"name":"Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen , Essen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Romy","family":"Barthel","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen , Essen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0178-2804","authenticated-orcid":false,"given":"Jasmin","family":"Bahr","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen , Essen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jacqueline","family":"Thiel","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen , Essen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sina","family":"Luppus","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen , Essen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7602-1698","authenticated-orcid":false,"given":"Jan","family":"Buer","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen , Essen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Astrid M","family":"Westendorf","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen , Essen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wiebke","family":"Hansen","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen , Essen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2021,9,1]]},"reference":[{"key":"2025022610320844700_r1","doi-asserted-by":"crossref","first-page":"477","DOI":"10.1038\/ni789","article-title":"A neuronal receptor, neuropilin-1, is essential for the initiation of the primary immune response. [Published erratum appears in 2003 Nat. Immunol. 4: 394.]","volume":"3","author":"Tordjman","year":"2002","journal-title":"Nat. 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