{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:52:27Z","timestamp":1787014347125,"version":"build-2736575974"},"reference-count":33,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2026,2,15]],"date-time":"2026-02-15T00:00:00Z","timestamp":1771113600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,2,15]],"date-time":"2026-02-15T00:00:00Z","timestamp":1771113600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Int J Immunogenetics"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disorder influenced by genetic and environmental factors. Vitamin D deficiency and vitamin D receptor (VDR) gene polymorphisms are suggested to modulate immune dysregulation in SLE. This study aimed to investigate the association of VDR polymorphisms (\n                    <jats:italic>BsmI<\/jats:italic>\n                    ,\n                    <jats:italic>ApaI<\/jats:italic>\n                    ,\n                    <jats:italic>TaqI<\/jats:italic>\n                    and\n                    <jats:italic>FokI<\/jats:italic>\n                    ), serum 25\u2010hydroxyvitamin D [25\u2010OH vitamin D] levels and clinical phenotypes in Indian SLE patients. A hospital\u2010based case\u2013control study was conducted on clinically diagnosed SLE patients (\n                    <jats:italic>n<\/jats:italic>\n                    \u00a0=\u00a0297) fulfilling American College of Rheumatology (ACR) criteria and healthy controls (\n                    <jats:italic>n<\/jats:italic>\n                    \u00a0=\u00a0100). Serum 25\u2010OH vitamin D levels, autoantibody profile and complement components were evaluated by immunofluorescence, enzyme\u2010linked immunosorbent assay (ELISA) and nephelometry. Genotyping for VDR polymorphisms\n                    <jats:italic>BsmI<\/jats:italic>\n                    (rs1544410) B\/b,\n                    <jats:italic>ApaI<\/jats:italic>\n                    (rs7975232) A\/a,\n                    <jats:italic>TaqI<\/jats:italic>\n                    (rs731236) T\/t and\n                    <jats:italic>FokI<\/jats:italic>\n                    (rs2228570) F\/f was performed using polymerase chain reaction\u2010restriction fragment length polymorphism (PCR\u2010RFLP). Data were statistically analysed using chi\u2010square tests, logistic regression and correlation analysis. The median age at evaluation in SLE patients was 29 years, with a female predominance (91.9%). Median serum 25\u2010OH vitamin D levels were 30.4\u00a0ng\/mL, with lower levels observed in patients with arthritis (\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0=\u00a00.012), neurological involvement (\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0=\u00a00.015) and active disease (\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0=\u00a00.025). Serum 25\u2010OH vitamin D inversely correlated with disease activity (\n                    <jats:italic>r<\/jats:italic>\n                    \u00a0=\u00a0\u22120.127,\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0=\u00a00.032), anti\u2010cardiolipin antibody (ACLA) immunoglobulin G (IgG) (\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0&lt;\u00a00.001) and anti\u2010phospholipid antibody (APLA) IgG (\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0=\u00a00.030). Among VDR polymorphisms,\n                    <jats:italic>BsmI<\/jats:italic>\n                    b allele conferred reduced disease risk (odds ratio [OR]\u00a0=\u00a01.85,\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0&lt;\u00a00.001).\n                    <jats:italic>TaqI<\/jats:italic>\n                    genotypes (Tt: OR\u00a0=\u00a02.29 and tt: OR\u00a0=\u00a06.48,\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0&lt;\u00a00.05) and t allele (OR\u00a0=\u00a02.15,\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0&lt;\u00a00.001) and\n                    <jats:italic>FokI<\/jats:italic>\n                    genotypes (Ff: OR\u00a0=\u00a04.13 and ff: OR\u00a0=\u00a03.14,\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0&lt;0.05) were strongly associated with increased susceptibility to SLE.\n                    <jats:italic>ApaI<\/jats:italic>\n                    variants were significantly associated with alopecia, haematological manifestations, disease activity and low complement component 3 (C3) levels, whereas\n                    <jats:italic>BsmI<\/jats:italic>\n                    and\n                    <jats:italic>FokI<\/jats:italic>\n                    polymorphisms were associated with neurological manifestations (\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0&lt;\u00a00.05). Vitamin D receptor gene (VDR gene) polymorphisms may contribute to phenotypic variability and immune dysregulation in Indian SLE patients, suggesting that gene\u2013environment interactions between vitamin D status and VDR variants may influence SLE susceptibility and clinical heterogeneity.\n                  <\/jats:p>","DOI":"10.1111\/iji.70042","type":"journal-article","created":{"date-parts":[[2026,2,16]],"date-time":"2026-02-16T05:12:44Z","timestamp":1771218764000},"page":"179-192","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Elucidating the Role of Vitamin D Receptor (VDR) Polymorphisms in Genetic Susceptibility to Systemic Lupus Erythematosus: A Case\u2010Control Study From Western India"],"prefix":"10.1111","volume":"53","author":[{"given":"Swapnal","family":"Pawaskar","sequence":"first","affiliation":[{"name":"Department of Clinical &amp; Experimental Immunology Indian Council of Medical Research\u2013National Institute of Immunohaematology  Parel, Mumbai India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Durga","family":"Chougule","sequence":"additional","affiliation":[{"name":"Department of Clinical &amp; Experimental Immunology Indian Council of Medical Research\u2013National Institute of Immunohaematology  Parel, Mumbai India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amrutha","family":"Jose","sequence":"additional","affiliation":[{"name":"Department of Haematogenetics Indian Council of Medical Research\u2013National Institute of Immunohaematology  Parel, Mumbai India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anjali","family":"Rajadhyaksha","sequence":"additional","affiliation":[{"name":"Department of Medicine G.S. 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