{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T18:07:54Z","timestamp":1784743674295,"version":"3.55.0"},"reference-count":18,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2020,2,18]],"date-time":"2020-02-18T00:00:00Z","timestamp":1581984000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2020,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The sphingolipid sphingosine\u20101\u2010phosphate (S1P) fulfills distinct functions in immune cell biology via binding to five G protein\u2010coupled receptors. The immune cell\u2010specific sphingosine\u20101\u2010phosphate receptor 4 (S1pr4) was connected to the generation of IL\u201017\u2010producing T cells through regulation of cytokine production in innate immune cells. Therefore, we explored whether S1pr4 affected imiquimod\u2010induced murine psoriasis via regulation of IL\u201017 production. We did not observe altered IL\u201017 production, although psoriasis severity was reduced in S1pr4\u2010deficient mice. Instead, ablation of S1pr4 attenuated the production of CCL2, IL\u20106, and CXCL1 and subsequently reduced the number of infiltrating monocytes and granulocytes. A connection between S1pr4, CCL2, and M\u03d5 infiltration was also observed in Zymosan\u2010A induced peritonitis. Boyden chamber migration assays functionally linked reduced CCL2 production in murine skin and attenuated monocyte migration when S1pr4 was lacking. Mechanistically, S1pr4 signaling synergized with TLR signaling in resident M\u03d5s to produce CCL2, likely via the NF\u2010\u03baB pathway. We propose that S1pr4 activation enhances TLR response of resident M\u03d5s to increase CCL2 production, which attracts further M\u03d5s. Thus, S1pr4 may be a target to reduce perpetuating inflammatory responses.<\/jats:p>","DOI":"10.1002\/eji.201948349","type":"journal-article","created":{"date-parts":[[2020,2,4]],"date-time":"2020-02-04T07:53:14Z","timestamp":1580802794000},"page":"839-845","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["S1PR4\u2010dependent CCL2 production promotes macrophage recruitment in a murine psoriasis model"],"prefix":"10.1002","volume":"50","author":[{"given":"Christian","family":"Schuster","sequence":"first","affiliation":[{"name":"Institute of Biochemistry I Faculty of Medicine Goethe\u2010University Frankfurt  60590 Frankfurt Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arnaud","family":"Huard","sequence":"additional","affiliation":[{"name":"Institute of Biochemistry I Faculty of Medicine Goethe\u2010University Frankfurt  60590 Frankfurt 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