{"entity": "researcher", "timestamp": "2026-09-23T15:23:34.317Z", "family": "Leonard", "given": "Dag", "initials": "D", "orcid": "0000-0002-6275-7282", "affiliations": ["Rheumatology and Science for Life Laboratory, Department of Medical Sciences, Uppsala University, Uppsala, Sweden."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/444ae7021f634df8b55e61c85c81b28b.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/444ae7021f634df8b55e61c85c81b28b"}}, "publications": [{"entity": "publication", "iuid": "9ad12fdc9ed942cb8ea5052646fabe08", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/9ad12fdc9ed942cb8ea5052646fabe08.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/9ad12fdc9ed942cb8ea5052646fabe08"}}, "title": "Genetic risk factors and clinical manifestations of systemic lupus erythematosus: Large-scale analysis of genetic predisposition and disease subtypes.", "authors": [{"family": "Reid", "given": "Sarah", "initials": "S"}, {"family": "Sandling", "given": "Johanna K", "initials": "JK", "orcid": "0000-0003-1382-2321", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c5bbdb0cf40c48198ea04ede2fb33377.json"}}, {"family": "Pucholt", "given": "Pascal", "initials": "P"}, {"family": "Sayadi", "given": "Ahmed", "initials": "A"}, {"family": "Frodlund", "given": "Martina", "initials": "M"}, {"family": "Lerang", "given": "Karoline", "initials": "K"}, {"family": "Gunnarsson", "given": "Iva", "initials": "I"}, {"family": "J\u00f6nsen", "given": "Andreas", "initials": "A"}, {"family": "Syv\u00e4nen", "given": "Ann-Christine", "initials": "AC"}, {"family": "Molberg", "given": "\u00d8yvind", "initials": "\u00d8"}, {"family": "Rantap\u00e4\u00e4-Dahlqvist", "given": "Solbritt", "initials": "S", "orcid": "0000-0001-8259-3863", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1c8c4d669b3942309a148980c1437b5d.json"}}, {"family": "Rudin", "given": "Anna", "initials": "A", "orcid": "0000-0002-4137-1276", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/87a26237ea1f43e4a911a2c8d21c8d4a.json"}}, {"family": "Sj\u00f6wall", "given": "Christopher", "initials": "C", "orcid": "0000-0003-0900-2048", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a9fcc24622ec440bac6996072cceea0e.json"}}, {"family": "Svenungsson", "given": "Elisabet", "initials": "E", "orcid": "0000-0003-3396-3244", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2c44ebd4f33e46a1862877bce94be05b.json"}}, {"family": "Bengtsson", "given": "Anders A", "initials": "AA"}, {"family": "R\u00f6nnblom", "given": "Lars", "initials": "L", "orcid": "0000-0001-9403-6503", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5f7ec7a7befd44cc988091ba0858d3c0.json"}}, {"family": "Leonard", "given": "Dag", "initials": "D", "orcid": "0000-0002-6275-7282", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/444ae7021f634df8b55e61c85c81b28b.json"}}], "type": "journal article", "published": "2026-01-00", "journal": {"title": "J. Intern. Med.", "issn": "1365-2796", "volume": "299", "issue": "1", "pages": "95-108", "issn-l": "0954-6820"}, "abstract": "Systemic lupus erythematosus (SLE) is an autoimmune disease with a heterogenous clinical picture. This study aimed to link genetic SLE predisposition with relevant clinical manifestations.\n\nDatasets best corresponding to the 11 American College of Rheumatology 1982 (ACR-82) classification criteria for SLE in a large, public database (FinnGen consortium, >218,000 individuals) were identified. Mendelian randomization analysis was conducted to evaluate the effect of a high genetic SLE predisposition on each manifestation. Next, validation was conducted in a clinical SLE cohort comprising 1487 genotyped Scandinavian patients with detailed clinical data. Based on the public datasets, genetic risk scores (GRSs) for each relevant manifestation were constructed for each patient. Associations between each GRS and the corresponding ACR-82 criterion were evaluated using logistic regression.\n\nIn the FinnGen biobank, the cumulative effect of the 57 SLE risk SNPs was associated with an increased risk of rosacea, OR 1.09 (1.03-1.16), polyarthropathies, OR 1.10 (1.06-1.14), pleural effusions, OR 1.09 (1.04-1.14), and hemolytic anemia, OR 1.32 (1.10-1.58). In the clinical cohort, 5 of the 11 GRSs generated from the public datasets were associated with their corresponding ACR-82 criterion: arthritis, OR 1.15 (1.02-1.31), renal disorder, OR 1.15 (1.04-1.29), neurologic disorder, OR 1.24 (1.04-1.47), hematologic disorder, OR 1.12 (1.00-1.24), and immunologic disorder, OR 1.37 (1.22-1.56).\n\nThe findings demonstrate that known SLE risk gene variants play a role in the development of at least half of the ACR-82 criteria for SLE, indicating a future possibility of using genetics to predict a variety of disease sub-phenotypes in SLE.", "doi": "10.1111/joim.70040", "pmid": "41200769", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC12678220"}], "notes": [], "created": "2026-09-23T12:36:07.836Z", "modified": "2026-09-23T12:36:07.972Z"}, {"entity": "publication", "iuid": "e5df78fc82614b54a5b51d9384a17abe", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/e5df78fc82614b54a5b51d9384a17abe.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/e5df78fc82614b54a5b51d9384a17abe"}}, "title": "A high polygenic risk score is associated with SSA/SSB antibody positivity and early onset in primary Sj\u00f6gren's disease.", "authors": [{"family": "Fugmann", "given": "Cecilia", "initials": "C", "orcid": "0009-0005-6078-8826", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/040e76f2cde44590b1c3f9318f27ab18.json"}}, {"family": "Reid", "given": "Sarah", "initials": "S"}, {"family": "Pucholt", "given": "Pascal", "initials": "P", "orcid": "0000-0003-3342-1373", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b8d564c4e36f451f9b78f563c9e8fa07.json"}}, {"family": "Kvarnstr\u00f6m", "given": "Marika", "initials": "M"}, {"family": "Bj\u00f6rk", "given": "Albin", "initials": "A"}, {"family": "Mofors", "given": "Johannes", "initials": "J", "orcid": "0000-0003-1873-7169", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6bae04084cd840959d659f12c5197462.json"}}, {"family": "Sj\u00f6wall", "given": "Christopher", "initials": "C", "orcid": "0000-0003-0900-2048", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a9fcc24622ec440bac6996072cceea0e.json"}}, {"family": "Eriksson", "given": "Per", "initials": "P"}, {"family": "Olsson", "given": "Peter", "initials": "P"}, {"family": "Mandl", "given": "Thomas", "initials": "T", "orcid": "0000-0002-7143-7088", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a3ae58ec5cc8471f91b1f5a23295df29.json"}}, {"family": "Forsblad-d'Elia", "given": "Helena", "initials": "H", "orcid": "0000-0001-7871-5303", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6a995d1584ab4f0aaee7d12b4ba48006.json"}}, {"family": "Magnusson Bucher", "given": "Sara", "initials": "S"}, {"family": "Johnsen", "given": "Svein Joar", "initials": "SJ", "orcid": "0000-0002-1591-9250", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c7aa8dc8c5624dc49c03ee71cb9f1960.json"}}, {"family": "Norheim", "given": "Katrine Br\u00e6kke", "initials": "KB"}, {"family": "Appel", "given": "Silke", "initials": "S", "orcid": "0000-0002-2199-2315", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/22291aef0c15471fadc39931c5c02094.json"}}, {"family": "Hammenfors", "given": "Daniel", "initials": "D"}, {"family": "Jensen", "given": "Janicke Liaaen", "initials": "JL", "orcid": "0000-0003-4276-9611", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/da5f017d5ba2439d892c8bede353a700.json"}}, {"family": "Palm", "given": "\u00d8yvind", "initials": "\u00d8"}, {"family": "Omdal", "given": "Roald", "initials": "R"}, {"family": "Jonsson", "given": "Roland", "initials": "R", "orcid": "0000-0002-9588-0260", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/03b77dc6eefa489c871580fc27089af6.json"}}, {"family": "Baecklund", "given": "Eva", "initials": "E", "orcid": "0000-0001-5033-0188", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/7317920dadc545a6bacdcb61f07e2cdb.json"}}, {"family": "Wahren-Herlenius", "given": "Marie", "initials": "M", "orcid": "0000-0002-0915-7245", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0db5190dbe894a5e9cd961e66ba5c75d.json"}}, {"family": "Leonard", "given": "Dag", "initials": "D", "orcid": "0000-0002-6275-7282", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/444ae7021f634df8b55e61c85c81b28b.json"}}, {"family": "Imgenberg-Kreuz", "given": "Juliana", "initials": "J", "orcid": "0000-0002-7230-8990", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b94ba6e41ec348138bba169099da410d.json"}}, {"family": "Nordmark", "given": "Gunnel", "initials": "G", "orcid": "0000-0002-3829-7431", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f618934952594d76a747bcbe2c27bbf2.json"}}], "type": "journal article", "published": "2025-07-01", "journal": {"title": "Rheumatology (Oxford)", "issn": "1462-0332", "volume": "64", "issue": "7", "pages": "4341-4346", "issn-l": "1462-0324"}, "abstract": "To calculate a polygenic risk score (PRS) based on single nucleotide variants (SNVs) previously associated with primary Sj\u00f6gren's disease (SjD) with genome-wide significance and determine the genetic risk for SjD stratified by antibodies, sex and age at diagnosis.\n\nPatients with SjD (n = 1065) were genotyped using Illumina OmniExpressExome chip. Control genotype data were available (n = 7742). Two PRSs were constructed, one including HLA gene variants (n = 21 SNVs), and one without HLA (n = 18 SNVs). High PRS quartile (Q4) individuals were compared with low PRS (Q1-3).\n\nA high PRS was associated with SSA antibody-positive SjD (OR 9.16, 95% CI 7.75-10.85, P = 3.7 \u00d7 10-146), and strengthened in SjD positive for both SSA/SSB antibodies (OR 13.67, 95% CI 10.88-17.32, P = 4.6 \u00d7 10-108). High PRS classified SSA/SSB antibody-positive SjD with very good accuracy (AUC 0.86). PRS without HLA showed a weaker association with SSA/SSB positive SjD (OR 2.09, 95% CI 1.71-2.55, P = 6.4 \u00d7 10-13). Antibody negative SjD displayed a PRS similar to controls. Patients in the high PRS quartile were significantly younger at diagnosis, 48.9 \u00b1 14.9 vs 53.4 \u00b1 13.4 years in the low PRS quartiles (Q1-3), P = 2.2 \u00d7 10-6, and presented higher frequencies of ANA, SSA and SSA/SSB antibodies, P < 1 \u00d7 10-5.\n\nA high PRS is associated with SSA/SSB antibody positivity and early disease onset, both largely attributed to the weight of the HLA alleles. Integration of PRS with other biomarkers applied to clinical phenotypes could be a useful tool for disease risk stratification and treatment decisions.", "doi": "10.1093/rheumatology/keae693", "pmid": "39693120", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC12212914"}, {"db": "pii", "key": "7927842"}], "notes": [], "created": "2026-09-23T12:27:27.339Z", "modified": "2026-09-23T12:27:27.606Z"}, {"entity": "publication", "iuid": "5f5bd98bdc044b8faf1be206e871b7b2", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/5f5bd98bdc044b8faf1be206e871b7b2.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/5f5bd98bdc044b8faf1be206e871b7b2"}}, "title": "Mer-tyrosine kinase: a novel susceptibility gene for SLE related end-stage renal disease.", "authors": [{"family": "Yavuz", "given": "Sule", "initials": "S"}, {"family": "Pucholt", "given": "Pascal", "initials": "P", "orcid": "0000-0003-3342-1373", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b8d564c4e36f451f9b78f563c9e8fa07.json"}}, {"family": "Sandling", "given": "Johanna K", "initials": "JK", "orcid": "0000-0003-1382-2321", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c5bbdb0cf40c48198ea04ede2fb33377.json"}}, {"family": "Bianchi", "given": "Matteo", "initials": "M"}, {"family": "Leonard", "given": "Dag", "initials": "D", "orcid": "0000-0002-6275-7282", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/444ae7021f634df8b55e61c85c81b28b.json"}}, {"family": "Bolin", "given": "Karin", "initials": "K"}, {"family": "Imgenberg-Kreuz", "given": "Juliana", "initials": "J"}, {"family": "Eloranta", "given": "Maija-Leena", "initials": "ML"}, {"family": "Kozyrev", "given": "Sergey V", "initials": "SV", "orcid": "0000-0001-6209-4100", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/cef7ddc40d8f47468f3f3dec3caa5de3.json"}}, {"family": "Lanata", "given": "Cristina M", "initials": "CM"}, {"family": "J\u00f6nsen", "given": "Andreas", "initials": "A"}, {"family": "Bengtsson", "given": "Anders A", "initials": "AA"}, {"family": "Sj\u00f6wall", "given": "Christopher", "initials": "C", "orcid": "0000-0003-0900-2048", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a9fcc24622ec440bac6996072cceea0e.json"}}, {"family": "Svenungsson", "given": "Elisabet", "initials": "E", "orcid": "0000-0003-3396-3244", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2c44ebd4f33e46a1862877bce94be05b.json"}}, {"family": "Gunnarsson", "given": "Iva", "initials": "I"}, {"family": "Rantap\u00e4\u00e4-Dahlqvist", "given": "Solbritt", "initials": "S"}, {"family": "ImmunoArray Development Consortium", "given": "", "initials": ""}, {"family": "DISSECT Consortium", "given": "", "initials": ""}, {"family": "Nititham", "given": "Joanne", "initials": "J"}, {"family": "Criswell", "given": "Lindsey A", "initials": "LA"}, {"family": "Lindblad-Toh", "given": "Kerstin", "initials": "K"}, {"family": "R\u00f6nnblom", "given": "Lars", "initials": "L", "orcid": "0000-0001-9403-6503", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5f7ec7a7befd44cc988091ba0858d3c0.json"}}], "type": "meta-analysis", "published": "2022-11-00", "journal": {"title": "Lupus Sci Med", "issn": "2053-8790", "volume": "9", "issue": "1", "issn-l": null}, "abstract": "Lupus nephritis (LN) is a common and severe manifestation of SLE. The genetic risk for nephritis and progression to end-stage renal disease (ESRD) in patients with LN remains unclear. Herein, we aimed to identify novel genetic associations with LN, focusing on subphenotypes and ESRD.\n\nWe analysed genomic data on 958 patients with SLE (discovery cohort: LN=338) with targeted sequencing data from 1832 immunological pathway genes. We used an independent multiethnic cohort comprising 1226 patients with SLE (LN=603) as a replication dataset. Detailed functional annotation and functional epigenomic enrichment analyses were applied to predict functional effects of the candidate variants.\n\nA genetic variant (rs56097910) within the MERTK gene was associated with ESRD in both cohorts, meta-analysis OR=5.4 (2.8 to 10.6); p=1.0\u00d710-6. We observed decreased methylation levels in peripheral blood cells from SLE patients with ESRD, compared with patients without renal SLE (p=2.7\u00d710-4), at one CpG site (cg16333401) in close vicinity to the transcription start site of MERTK and located in a DNAse hypersensitivity region in T and B cells. Rs56097910 is linked to altered MERTK expression in kidney tissue in public eQTL databases. Two loci were replicated for association with proliferative LN: PRDM1 (rs6924535, pmeta=1.6\u00d710-5, OR=0.58) and APOA1BP (NAXE) (rs942960, pmeta=1.2\u00d710-5, OR=2.64).\n\nWe identified a novel genetic risk locus, MERTK, associated with SLE-ESRD using the data from two large SLE cohorts. Through DNA methylation analysis and functional annotation, we showed that the risk could be mediated through regulation of gene expression. Our results suggest that variants in the MERTK gene are important for the risk of developing SLE-ESRD and suggest a role for PRDM1 and APOA1BP in proliferative LN.", "doi": "10.1136/lupus-2022-000752", "pmid": "36332927", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9639142"}, {"db": "pii", "key": "9/1/e000752"}], "notes": [], "created": "2026-09-23T12:11:39.258Z", "modified": "2026-09-23T12:11:39.343Z"}, {"entity": "publication", "iuid": "b619642dacb342078ca7175000185e33", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/b619642dacb342078ca7175000185e33.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/b619642dacb342078ca7175000185e33"}}, "title": "High genetic risk score is associated with early disease onset, damage accrual and decreased survival in systemic lupus erythematosus.", "authors": [{"family": "Reid", "given": "Sarah", "initials": "S", "orcid": "0000-0003-4065-6875", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/dbb022bf9c044578923d23851f969208.json"}}, {"family": "Alexsson", "given": "Andrei", "initials": "A"}, {"family": "Frodlund", "given": "Martina", "initials": "M"}, {"family": "Morris", "given": "David", "initials": "D"}, {"family": "Sandling", "given": "Johanna K", "initials": "JK"}, {"family": "Bolin", "given": "Karin", "initials": "K"}, {"family": "Svenungsson", "given": "Elisabet", "initials": "E", "orcid": "0000-0003-3396-3244", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2c44ebd4f33e46a1862877bce94be05b.json"}}, {"family": "J\u00f6nsen", "given": "Andreas", "initials": "A"}, {"family": "Bengtsson", "given": "Christine", "initials": "C"}, {"family": "Gunnarsson", "given": "Iva", "initials": "I"}, {"family": "Illescas Rodriguez", "given": "Vera", "initials": "V"}, {"family": "Bengtsson", "given": "Anders", "initials": "A"}, {"family": "Arve", "given": "Sabine", "initials": "S", "orcid": "0000-0002-3347-5550", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5d063b42c4af42efbba4afb26b9a9fd3.json"}}, {"family": "Rantap\u00e4\u00e4-Dahlqvist", "given": "Solbritt", "initials": "S", "orcid": "0000-0001-8259-3863", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1c8c4d669b3942309a148980c1437b5d.json"}}, {"family": "Eloranta", "given": "Maija-Leena", "initials": "ML"}, {"family": "Syv\u00e4nen", "given": "Ann-Christine", "initials": "AC"}, {"family": "Sj\u00f6wall", "given": "Christopher", "initials": "C", "orcid": "0000-0003-0900-2048", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a9fcc24622ec440bac6996072cceea0e.json"}}, {"family": "Vyse", "given": "Timothy James", "initials": "TJ"}, {"family": "R\u00f6nnblom", "given": "Lars", "initials": "L", "orcid": "0000-0001-9403-6503", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5f7ec7a7befd44cc988091ba0858d3c0.json"}}, {"family": "Leonard", "given": "Dag", "initials": "D", "orcid": "0000-0002-6275-7282", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/444ae7021f634df8b55e61c85c81b28b.json"}}], "type": "journal article", "published": "2020-03-00", "journal": {"title": "Ann. Rheum. Dis.", "issn": "1468-2060", "volume": "79", "issue": "3", "pages": "363-369", "issn-l": "0003-4967"}, "abstract": "To investigate associations between a high genetic disease risk and disease severity in patients with systemic lupus erythematosus (SLE).\n\nPatients with SLE (n=1001, discovery cohort and n=5524, replication cohort) and healthy controls (n=2802 and n=9859) were genotyped using a 200K Immunochip single nucleotide polymorphism array. A genetic risk score (GRS) was assigned to each individual based on 57 SLE risk loci.\n\nSLE was more prevalent in the high, compared with the low, GRS-quartile (OR 12.32 (9.53 to 15.71), p=7.9\u00d710-86 and OR 7.48 (6.73 to 8.32), p=2.2\u00d710-304 for the discovery and the replication cohorts, respectively). In the discovery cohort, patients in the high GRS-quartile had a 6-year earlier mean disease onset (HR 1.47 (1.22 to 1.75), p=4.3\u00d710-5), displayed higher prevalence of damage accrual (OR 1.47 (1.06 to 2.04), p=2.0\u00d710-2), renal disorder (OR 2.22 (1.50 to 3.27), p=5.9\u00d710-5), anti-dsDNA (OR 1.83 (1.19 to 2.81), p=6.1\u00d710-3), end-stage renal disease (ESRD) (OR 5.58 (1.50 to 20.79), p=1.0\u00d710-2), proliferative nephritis (OR 2.42 (1.30 to 4.49), p=5.1\u00d710-3), anti-cardiolipin-IgG (OR 1.89 (1.13 to 3.18), p=1.6\u00d710-2), anti-\u03b22-glycoprotein-I-IgG (OR 2.29 (1.29 to 4.06), p=4.8\u00d710-3) and positive lupus anticoagulant test (OR 2.12 (1.16 to 3.89), p=1.5\u00d710-2) compared with patients in the low GRS-quartile. Survival analysis showed earlier onset of the first organ damage (HR 1.51 (1.04 to 2.25), p=3.7\u00d710-2), first cardiovascular event (HR 1.65 (1.03 to 2.64), p=2.6\u00d710-2), nephritis (HR 2.53 (1.72 to 3.71), p=9.6\u00d710-7), ESRD (HR 6.78 (1.78 to 26.86), p=6.5\u00d710-3) and decreased overall survival (HR 1.83 (1.02 to 3.30), p=4.3\u00d710-2) in high to low quartile comparison.\n\nA high GRS is associated with increased risk of organ damage, renal dysfunction and all-cause mortality. Our results indicate that genetic profiling may be useful for predicting outcomes in patients with SLE.", "doi": "10.1136/annrheumdis-2019-216227", "pmid": "31826855", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC7034364"}, {"db": "pii", "key": "S0003-4967(24)01473-0"}], "notes": [], "created": "2026-09-23T07:28:57.423Z", "modified": "2026-09-23T07:28:57.509Z"}]}