{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T09:07:14Z","timestamp":1780477634151,"version":"3.54.1"},"reference-count":62,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T00:00:00Z","timestamp":1780444800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Bioinform."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Rheumatoid Arthritis (RA) is characterized as a systemic, chronic inflammatory autoimmune condition that causes joints damage and bone deformities. Recent studies indicate that the Single Nucleotide Polymorphisms (SNPs) within the immunoregulatory genes like Fc receptor-like3 (\n                      <jats:italic>FCRL3<\/jats:italic>\n                      ) have a significant association with RA. The primary objective of this study is to explore the association between\n                      <jats:italic>FCRL3<\/jats:italic>\n                      gene variants and RA risk in 226 Indian RA patients compared to 239 controls.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Genotyping of\n                      <jats:italic>FCRL3<\/jats:italic>\n                      SNPs rs7522061, rs11264799, rs11264797, and rs7549100 was performed using High-Resolution Melting Analysis, followed by Sanger sequencing to validate the accuracy of the results. To assess the association between SNPs and RA, unadjusted odd ratios (ORs) with 95% Confidence Interval (CI), gender-stratified analyses, and multivariable logistic regression adjusted for age and sex were performed. Furthermore, to investigate the impact of rs7522061 SNP in RA pathogenesis, an\n                      <jats:italic>in silico<\/jats:italic>\n                      approach involving homology modelling and molecular docking (HADDOCK) of FCRL3 wild type vs. variant (N28D) protein with SHP-1 was employed and 1,000 ns?Coarse-Grained Molecular Dynamics (CG-MD) simulations (GROMACS\/MARTINI v3.0) was performed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The rs7522061 G\/A genotype was significantly associated with increased RA risk (unadjusted OR = 1.84, 95% CI = 1.21\u20132.79, adjusted\n                      <jats:italic>p =<\/jats:italic>\n                      0.0200). Multivariable logistic regression confirmed this association was independent of age and sex (adjusted OR = 2.03,\n                      <jats:italic>p =<\/jats:italic>\n                      0.0028).\n                      <jats:italic>In-silico<\/jats:italic>\n                      analysis revealed that the FCRL3 N28D variant formed a more favourable docking interface with SHP-1 (mean HADDOCK score: 61.1 \u00b1 11.0 vs. - 53.45 \u00b1 5.84) compared to wild type and 1,000 ns CG-MD stimulation exhibited faster equilibration, lower RMSD, tighter Interfacial distance (0.15 nm), more persistent interprotein contacts, and greater compactness.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      <jats:italic>FCRL3<\/jats:italic>\n                      SNP rs7522061 G\/A genotype contributes to RA susceptibility in the Indian population. The computational study suggests that the N28D substitution enhances FCRL3\u2013SHP-1 complex stability, which may disrupt Treg function through increased negative signalling.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fbinf.2026.1809854","type":"journal-article","created":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T08:13:31Z","timestamp":1780474411000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Association of FCRL3 gene variants with rheumatoid arthritis susceptibility in the indian population: a combined case-control and in- silico analysis"],"prefix":"10.3389","volume":"6","author":[{"given":"Mohamed","family":"Muzammil S","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences School of Bio Sciences and Technology, Vellore Institute of Technology","place":["Vellore, Tamil Nadu, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Asha","family":"Devi S","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences School of Bio Sciences and Technology, Vellore Institute of Technology","place":["Vellore, Tamil Nadu, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,6,3]]},"reference":[{"key":"B1","volume-title":"Predicting Functional Effect of Human Missense Variations Using PolyPhen-2","author":"Adzhubei","year":"2013"},{"key":"B2","doi-asserted-by":"publisher","first-page":"1292","DOI":"10.1016\/j.celrep.2019.12.099","article-title":"Human Fc receptor-like 3 inhibits regulatory T cell function and binds secretory IgA","volume":"30","author":"Agarwal","year":"2020","journal-title":"Cell Rep."},{"key":"B3","doi-asserted-by":"publisher","first-page":"3354","DOI":"10.1016\/j.sjbs.2020.08.045","article-title":"Association study of CCR6 rs3093024 with rheumatoid arthritis in a Pakistani cohort","volume":"27","author":"Akhtar","year":"2020","journal-title":"Saudi J. 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