{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T12:40:28Z","timestamp":1788784828702,"version":"build-2803163510"},"reference-count":80,"publisher":"MDPI AG","issue":"11","license":[{"start":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T00:00:00Z","timestamp":1762041600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes"],"abstract":"<jats:p>The pathogenesis of rheumatoid arthritis involves a complex interplay of genetic predisposition, environmental factors, and autoimmune mechanisms that lead to chronic inflammation of the synovial membrane. Fc-like receptor 3 (FcRL3) is a receptor encoded by the FCRL3 gene, located on the long arm of chromosome 1 at 1q23.1. Polymorphisms in the promoter region of FCRL3, rather than elsewhere in the gene, primarily affect the level of protein expression, which is of clinical significance. Understanding the structure of FcRL3, particularly in the context of genetic variants, is therefore important for elucidating the pathogenesis of autoimmune diseases. Detailed knowledge of the molecular architecture of immune receptors such as FcRL3 is also essential for advancing our understanding of immune function and for guiding the development of targeted therapeutic strategies in autoimmune disease. In this article, we discuss the role of FcRL3 in the pathophysiology and potential therapy of rheumatoid arthritis.<\/jats:p>","DOI":"10.3390\/genes16111318","type":"journal-article","created":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T13:22:36Z","timestamp":1762176156000},"page":"1318","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["The Role of Fc-like Receptor 3 in the Pathophysiology of Rheumatoid Arthritis"],"prefix":"10.3390","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8514-3259","authenticated-orcid":false,"given":"Pawe\u0142","family":"Dec","sequence":"first","affiliation":[{"name":"Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-6821-0086","authenticated-orcid":false,"given":"Paulina","family":"Plewa","sequence":"additional","affiliation":[{"name":"Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adam","family":"Kubisa","sequence":"additional","affiliation":[{"name":"Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6557-1208","authenticated-orcid":false,"given":"Andrzej","family":"Pawlik","sequence":"additional","affiliation":[{"name":"Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2025,11,2]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"18001","DOI":"10.1038\/nrdp.2018.1","article-title":"Rheumatoid Arthritis","volume":"4","author":"Smolen","year":"2018","journal-title":"Nat. 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