{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,9]],"date-time":"2026-05-09T10:44:31Z","timestamp":1778323471514,"version":"3.51.4"},"reference-count":34,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2024,1,16]],"date-time":"2024-01-16T00:00:00Z","timestamp":1705363200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"Grant-in-Aid for Scientific Research","award":["23500489"],"award-info":[{"award-number":["23500489"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,4,29]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>G protein\u2013coupled receptors (GPCRs) regulate many cellular processes in response to various stimuli, including light, hormones, neurotransmitters, and odorants, some of which play critical roles in innate and adaptive immune responses. However, the physiological functions of many GPCRs and the involvement of them in autoimmune diseases of the central nervous system remain unclear. Here, we demonstrate that GPR141, an orphan GPCR belonging to the class A receptor family, suppresses immune responses. High GPR141 messenger RNA levels were expressed in myeloid-lineage cells, including neutrophils (CD11b + Gr1+), monocytes (CD11b + Gr1\u2212Ly6C+ and CD11b + Gr1\u2212Ly6C\u2212), macrophages (F4\/80+), and dendritic cells (CD11c+). Gpr141 \u00a0\u2212\/\u2212 mice, which we independently generated, displayed almost no abnormalities in myeloid cell differentiation and compartmentalization in the spleen and bone marrow under steady-state conditions. However, Gpr141 deficiency exacerbated disease conditions of experimental autoimmune encephalomyelitis, an autoimmune disease model for multiple sclerosis, with increased inflammation in the spinal cord. Gpr141 \u00a0\u2212\/\u2212 mice showed increased CD11b + Gr1+ neutrophils, CD11b + Gr1\u2212 monocytes, CD11c+ dendritic cells, and CD4+ T cell infiltration into the experimental autoimmune encephalomyelitis\u2013induced spinal cord compared with littermate control mice. Lymphocytes enriched from Gpr141 \u00a0\u2212\/\u2212 mice immunized with myelin oligodendrocyte glycoprotein 35\u201355 produced high amounts of interferon-\u03b3, interleukin-17A, and interleukin-6 compared with those from wild-type mice. Moreover, CD11c+ dendritic cells (DCs) purified from Gpr141 \u00a0\u2212\/\u2212 mice increased cytokine production of myelin oligodendrocyte glycoprotein 35\u201355\u2013specific T cells. These findings suggest that GPR141 functions as a negative regulator of immune responses by controlling the functions of monocytes and dendritic cells and that targeting GPR141 may be a possible therapeutic intervention for modulating chronic inflammatory diseases.<\/jats:p>","DOI":"10.1093\/jleuko\/qiae009","type":"journal-article","created":{"date-parts":[[2024,1,16]],"date-time":"2024-01-16T12:07:05Z","timestamp":1705406825000},"page":"935-945","source":"Crossref","is-referenced-by-count":8,"title":["The orphan G protein\u2013coupled receptor 141 expressed in myeloid cells functions as an inflammation suppressor"],"prefix":"10.1093","volume":"115","author":[{"given":"Atsuya","family":"Sawabe","sequence":"first","affiliation":[{"name":"Division of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University , 1-15-1, Fukumuro, Sendai 983-8536 , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shogo","family":"Okazaki","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Nihon University School of Dentistry , 1-8-13, Surugadai, Kanda, Chiyoda-ku, Tokyo 101-8310 , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Akira","family":"Nakamura","sequence":"additional","affiliation":[{"name":"Division of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University , 1-15-1, Fukumuro, Sendai 983-8536 , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ryo","family":"Goitsuka","sequence":"additional","affiliation":[{"name":"Division of Cell Fate Regulations, Developmental Immmunology, Regenerative Biology, Research Institute for Biomedical Sciences, Tokyo University of Science , 2669 Yamazaki, Noda, Chiba 278-0022 , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2614-1472","authenticated-orcid":false,"given":"Tomonori","family":"Kaifu","sequence":"additional","affiliation":[{"name":"Division of Immunology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University , 1-15-1, Fukumuro, Sendai 983-8536 , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2024,1,16]]},"reference":[{"key":"2024042918514226400_qiae009-B1","doi-asserted-by":"crossref","first-page":"533388","DOI":"10.3389\/fneur.2020.533388","article-title":"The role of antibodies in the pathogenesis of multiple sclerosis","volume":"11","author":"Yu","year":"2020","journal-title":"Front Neurol"},{"issue":"9","key":"2024042918514226400_qiae009-B2","doi-asserted-by":"crossref","first-page":"545","DOI":"10.1038\/nri3871","article-title":"Immunopathology of multiple 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