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"https://publications-affiliated.scilifelab.se/researcher/579f2ac07d8b45a2a57fad65d4ba5f5f.json"}}, {"family": "Wahren-Herlenius", "given": "Marie", "initials": "M", "orcid": "0000-0002-0915-7245", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0db5190dbe894a5e9cd961e66ba5c75d.json"}}, {"family": "Woessmann", "given": "Jakob", "initials": "J", "orcid": "0000-0002-2283-7237", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8a4b10f5f96244b98122eddcee694ec0.json"}}, {"family": "Yang", "given": "Hong", "initials": "H", "orcid": "0009-0002-0414-2471", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5f6b6c1901bc4c4daf3101f3de8b7029.json"}}, {"family": "Ye\u015filkaya", "given": "Umit Haluk", "initials": "UH"}, {"family": "Yuan", "given": "Meng", "initials": "M", "orcid": "0000-0002-9248-3294", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6fe547a601454a23acb16b1952400baf.json"}}, {"family": "Zeybel", "given": "Mujdat", "initials": "M", "orcid": "0000-0001-5440-4623", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a7bfd631ded14746be0b94b8f1cac968.json"}}, {"family": "Zhang", "given": "Cheng", "initials": "C", "orcid": "0000-0002-3721-8586", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f46e4161be08458994efddb75ed75874.json"}}, {"family": "Zhong", "given": "Wen", "initials": "W", "orcid": "0000-0002-7422-6104", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d6ffb1140aaa42c5ac63fe76653fc63b.json"}}, {"family": "Zwahlen", "given": "Martin", "initials": "M", "orcid": "0000-0002-0064-4776", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/456805fa3f4f47328f3923b78bf66996.json"}}, {"family": "von Feilitzen", "given": "Kalle", "initials": "K", "orcid": "0000-0002-0257-7554", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f4c4545bd2324b7d9b6696dab5bcb7dd.json"}}, {"family": "Nilsson", "given": "Peter", "initials": "P", "orcid": "0000-0002-4657-8532", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3db33fa3edb94febb8be7927a16838d0.json"}}, {"family": "Edfors", "given": "Fredrik", "initials": "F", "orcid": "0000-0002-0017-7987", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9e213b04f8984c8eb00c68f5bc2f6a36.json"}}, {"family": "Uhl\u00e9n", "given": "Mathias", "initials": "M", "orcid": "0000-0002-4858-8056", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9ea446aa574042a295d5f69437402f76.json"}}], "type": "journal article", "published": "2025-12-18", "journal": {"title": "Science (New York, N.Y.)", "issn": "1095-9203", "volume": "390", "issue": "6779", "pages": "eadx2678", "issn-l": "0036-8075"}, "abstract": "The human blood proteome provides a holistic readout of health states through the assessment of thousands of circulating proteins. In this study, we present a pan-disease resource to enable the study of diverse disease phenotypes within a harmonized proteomics dataset. By profiling protein concentrations across 59 diseases and healthy cohorts, we identified proteins associated with age, sex, and body mass index, as well as disease-specific signatures. This study highlights shared and distinct protein patterns across conditions, demonstrating the power of a unified proteomics approach to uncover biological insights. The dataset, covering 8262 individuals and up to 5416 proteins, serves as an online resource for exploring disease-specific protein profiles and advancing precision medicine research.", "doi": "10.1126/science.adx2678", "pmid": "41066540", "labels": {"SciLifeLab Fellow": "", "Adil Mardinoglu": ""}, "xrefs": [], "notes": [], "created": "2026-09-23T08:47:54.949Z", "modified": "2026-09-23T08:47:57.223Z"}, {"entity": "publication", "iuid": "802b4d38eda945dea38c11481e23dd9f", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/802b4d38eda945dea38c11481e23dd9f.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/802b4d38eda945dea38c11481e23dd9f"}}, "title": "Idiopathic inflammatory myopathies lack neutralising autoantibodies to type- I, II and III interferons.", "authors": [{"family": "Behere", "given": "Anish", "initials": "A", "orcid": "0000-0002-2424-3475", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c220e32442f343deb55eb3a1aa1865e0.json"}}, {"family": "Mildner", "given": "Hedvig", "initials": "H"}, {"family": "Peralta Garcia", "given": "Irene", "initials": "I"}, {"family": "P\u00e9rez Bucio", "given": "C\u00e9sar", "initials": "C"}, {"family": "Lundberg", "given": "Ingrid", "initials": "I", "orcid": "0000-0002-6068-9212", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a2891140c49d446dbd82c96857bcde73.json"}}, {"family": "Horuluoglu", "given": "Begum", "initials": "B"}, {"family": "Landegren", "given": "Nils", "initials": "N"}], "type": "journal article", "published": "2025-09-25", "journal": {"title": "RMD Open", "issn": "2056-5933", "volume": "11", "issue": "3", "issn-l": null}, "abstract": "To determine whether autoantibodies against interferons are present and play a role in disease modulation in idiopathic inflammatory myopathies (IIMs).\n\nWe screened for autoantibodies against a large number of interferons (IFNs) and other cytokines in a cross-sectional observational cohort of Swedish patients with anti-synthetase syndrome (n=51) and dermatomyositis (n=48), matched together with blood donors (n=100) from general population, using both planar and suspension-based multiplex assays. A single patient with autoimmune polyendocrine syndrome, type-1 (APS-1), known to harbour autoantibodies that neutralise type-I interferons, was included as a reference biological positive. The functional ability of autoantibodies to neutralise type-I interferons was tested in vitro, using an IFN-\u03b1/\u03b2 responsive cell reporter assay.\n\nThe initial screening of plasma samples indicated a repertoire of autoantibodies in IIM patients against a number of common myositis-specific and myositis-associated antigens. On screening for autoantibodies against type-I, II or III interferons, we did not find any evidence of anti-IFN autoantibodies being present in any of the IIM patient subgroups or the blood donors from general population. Additionally, none of the tested plasma samples, except the APS-1, exhibited neutralisation of physiological concentration IFN-\u03b12, further confirming a complete lack of functional autoantibodies against IFN-\u03b1 subtypes in this cohort.\n\nWe did not detect neutralising autoantibodies against IFN-\u03b1 and autoantibodies against other types of IFNs in a Swedish cohort of IIM patients. These findings contrast with the presence of autoantibodies against type-I IFNs in other systemic autoimmune diseases, such as systemic lupus erythematosus, characterised by type-I IFN overactivation.", "doi": "10.1136/rmdopen-2025-005836", "pmid": "40998521", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC12481268"}, {"db": "pii", "key": "rmdopen-2025-005836"}], "notes": [], "created": "2026-09-23T12:35:45.217Z", "modified": "2026-09-23T12:35:45.283Z"}, {"entity": "publication", "iuid": "0cb94737dbfe4b8784ca738e2b183430", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/0cb94737dbfe4b8784ca738e2b183430.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/0cb94737dbfe4b8784ca738e2b183430"}}, "title": "Anti-FHL1 autoantibodies in adult patients with myositis: a longitudinal follow-up analysis.", "authors": [{"family": "Galindo-Feria", "given": "Angeles S", "initials": "AS", "orcid": "0000-0001-7095-211X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/7be5528257ac4b4ead8dc05920e0a095.json"}}, {"family": "Lodin", "given": "Karin", "initials": "K"}, {"family": "Horuluoglu", "given": "Begum", "initials": "B"}, {"family": "Sarrafzadeh-Zargar", "given": "Sepehr", "initials": "S"}, {"family": "Wigren", "given": "Edvard", "initials": "E"}, {"family": "Gr\u00e4slund", "given": "Susanne", "initials": "S"}, {"family": "Danielsson", "given": "Olof", "initials": "O"}, {"family": "Wahren-Herlenius", "given": "Marie", "initials": "M", "orcid": "0000-0002-0915-7245", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0db5190dbe894a5e9cd961e66ba5c75d.json"}}, {"family": "Dastmalchi", "given": "Maryam", "initials": "M"}, {"family": "Lundberg", "given": "Ingrid E", "initials": "IE", "orcid": "0000-0002-6068-9212", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a2891140c49d446dbd82c96857bcde73.json"}}, {"family": "SweMyoNet Consortium", "given": "", "initials": ""}], "type": "journal article", "published": "2025-03-01", "journal": {"title": "Rheumatology (Oxford)", "issn": "1462-0332", "volume": "64", "issue": "3", "pages": "1482-1492", "issn-l": "1462-0324"}, "abstract": "To determine prevalence and clinical associations of anti-Four-and-a-half-LIM-domain 1 (FHL1) autoantibodies in patients with idiopathic inflammatory myopathies (IIM) and to evaluate autoantibody levels over time.\n\nSera at the time of diagnosis from patients with IIM (n = 449), autoimmune disease controls (DC, n = 130), neuromuscular diseases (NMDs, n = 16) and healthy controls (HC, n = 100) were analysed for anti-FHL1 autoantibodies by enzyme-linked immunosorbent assay (ELISA). Patients with IIM FHL1+ and FHL1- were included in a longitudinal analysis. Serum levels were correlated to disease activity.\n\nAutoantibodies to FHL1 were more frequent in patients with IIM (122/449, 27%) compared with DC (autoimmune DC and NMD, 13/146, 9%, P < 0.001) and HC (3/100.3%, P < 0.001). Anti-FHL1 levels were higher in IIM [median (IQR)=0.62 (0.15-1.04)] in comparison with DC [0.22 (0.08-0.58)], HC [0.35 (0.23-0.47)] and NMD [0.48 (0.36-0.80)] P < 0.001. Anti-FHL1+ patients with IIM were younger at the time of diagnosis compared with the anti-FHL1- group (P = 0.05) and were seronegative for other autoantibodies in 25%.In the first follow-up, anti-FHL1+ sample 20/33 (60%) positive at baseline had turned negative for anti-FHL1 autoantibodies. Anti-FHL1 autoantibodies rarely appeared after initiating treatment. Anti-FHL1 autoantibody levels correlated with CK (r = 0.62, P= 0.01), disease activity measured using the Myositis Disease Activity Assessment Tool (MYOACT) (n = 14, P = 0.004) and inversely with Manual Muscle Test-8 (r = -0.59, P = 0.02) at baseline.\n\nAnti-FHL1 autoantibodies were present in 27% of patients with IIM; of these, 25% were negative for other autoantibodies. Other autoimmune diseases had lower frequencies and levels. Anti-FHL1 levels often decreased with immunosuppressive treatment, correlated with disease activity measures at diagnosis and rarely appeared after start of treatment.", "doi": "10.1093/rheumatology/keae317", "pmid": "38833674", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11879316"}, {"db": "pii", "key": "7687810"}], "notes": [], "created": "2026-09-23T12:29:22.344Z", "modified": "2026-09-23T12:29:22.372Z"}, {"entity": "publication", "iuid": "f8942a7836cc47c9ac266895832ee8f9", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/f8942a7836cc47c9ac266895832ee8f9.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/f8942a7836cc47c9ac266895832ee8f9"}}, "title": "Unraveling the Genetics of Shared Clinical and Serological Manifestations in Patients With Systemic Inflammatory Autoimmune Diseases.", "authors": [{"family": "Bianchi", "given": "Matteo", "initials": "M", "orcid": "0000-0003-3394-6495", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3183e335a393486f8b6534db17b066d0.json"}}, {"family": "Kozyrev", "given": "Sergey V", "initials": "SV", "orcid": "0000-0001-6209-4100", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/cef7ddc40d8f47468f3f3dec3caa5de3.json"}}, {"family": "Notarnicola", "given": "Antonella", "initials": "A", "orcid": "0000-0003-0272-2931", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/708cd9cafb384ed29732f2c5fb1a17bd.json"}}, {"family": "Sandling", "given": "Johanna K", "initials": "JK"}, {"family": "Pettersson", "given": "Mats", "initials": "M"}, {"family": "Leonard", "given": "Dag", "initials": "D"}, {"family": "Sj\u00f6wall", "given": "Christopher", "initials": "C", "orcid": "0000-0003-0900-2048", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a9fcc24622ec440bac6996072cceea0e.json"}}, {"family": "Gunnarsson", "given": "Iva", "initials": "I"}, {"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": "Bengtsson", "given": "Anders A", "initials": "AA"}, {"family": "J\u00f6nsen", "given": "Andreas", "initials": "A"}, {"family": "Svenungsson", "given": "Elisabet", "initials": "E", "orcid": "0000-0003-3396-3244", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2c44ebd4f33e46a1862877bce94be05b.json"}}, {"family": "Enocsson", "given": "Helena", "initials": "H", "orcid": "0000-0002-2125-2931", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/174462ef4f7c4f6381aa2fd4cc29569d.json"}}, {"family": "Kvarnstr\u00f6m", "given": "Marika", "initials": "M"}, {"family": "Forsblad-d'Elia", "given": "Helena", "initials": "H"}, {"family": "Bucher", "given": "Sara Magnusson", "initials": "SM"}, {"family": "Norheim", "given": "Katrine B", "initials": "KB"}, {"family": "Baecklund", "given": "Eva", "initials": "E"}, {"family": "Jonsson", "given": "Roland", "initials": "R"}, {"family": "Hammenfors", "given": "Daniel", "initials": "D"}, {"family": "Eriksson", "given": "Per", "initials": "P"}, {"family": "Mandl", "given": "Thomas", "initials": "T"}, {"family": "Omdal", "given": "Roald", "initials": "R"}, {"family": "Padyukov", "given": "Leonid", "initials": "L"}, {"family": "Andersson", "given": "Helena", "initials": "H"}, {"family": "Molberg", "given": "\u00d8yvind", "initials": "\u00d8"}, {"family": "Diederichsen", "given": "Louise Pyndt", "initials": "LP"}, {"family": "Syv\u00e4nen", "given": "Ann-Christine", "initials": "AC"}, {"family": "Wahren-Herlenius", "given": "Marie", "initials": "M", "orcid": "0000-0002-0915-7245", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0db5190dbe894a5e9cd961e66ba5c75d.json"}}, {"family": "Nordmark", "given": "Gunnel", "initials": "G", "orcid": "0000-0002-3829-7431", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f618934952594d76a747bcbe2c27bbf2.json"}}, {"family": "Lundberg", "given": "Ingrid E", "initials": "IE", "orcid": "0000-0002-6068-9212", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a2891140c49d446dbd82c96857bcde73.json"}}, {"family": "R\u00f6nnblom", "given": "Lars", "initials": "L"}, {"family": "Lindblad-Toh", "given": "Kerstin", "initials": "K"}, {"family": "with the DISSECT consortium and the ImmunoArray consortium", "given": "", "initials": ""}], "type": "journal article", "published": "2025-02-00", "journal": {"title": "Arthritis & rheumatology (Hoboken, N.J.)", "issn": "2326-5205", "volume": "77", "issue": "2", "pages": "212-225", "issn-l": "2326-5191"}, "abstract": "Systemic inflammatory autoimmune diseases (SIADs) such as systemic lupus erythematosus (SLE), primary Sj\u00f6gren disease (pSS), and idiopathic inflammatory myopathies (myositis) are complex conditions characterized by shared circulating autoantibodies and clinical manifestations, including skin rashes, among others. This study was aimed at elucidating the genetics underlying these common features.\n\nWe performed targeted DNA sequencing of coding and regulatory regions from approximately 1,900 immune-related genes in a large cohort of 2,292 well-characterized Scandinavian patients with SIADs with SLE, pSS, and myositis as well as 1,252 controls. A gene-based functionally weighted genetic score for aggregate testing of all genetic variants, including rare variants, was complemented by in silico functional analyses and in vitro reporter experiments.\n\nCase-control association analysis detected known and potentially novel genetic loci in agreement with previous genetic and transcriptomics findings linked to the SIAD autoimmune background. Intriguingly, case-case comparisons between patient subgroups with and without specific autoantibodies revealed that the subgroups defined by antinuclear antibodies and anti-double-stranded DNA antibodies have unique genetic profiles reflecting their heterogeneity. When focusing on clinical features, we overall showed that dual-specificity phosphatase 1 (DUSP1) protective genetic variants lead to increased gene expression and potentially to anti-inflammatory effects on the SIAD-associated skin phenotype. This is consistent with recent genetic findings on eczema and with the previously reported down-regulation of the MAPK signaling-related gene DUSP1 in other skin disorders.\n\nTogether, this suggests common molecular mechanisms potentially underlying overlapping clinical manifestations shared among different disorders and informs clinical heterogeneity, which could be translated to improve disease diagnostic and treatment, also in more generalized disease frameworks.", "doi": "10.1002/art.42988", "pmid": "39284741", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11782108"}], "notes": [], "created": "2026-09-23T12:19:32.987Z", "modified": "2026-09-23T12:19:33.106Z"}, {"entity": "publication", "iuid": "e1ece15c11e14b8d8cd0d18214fda961", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/e1ece15c11e14b8d8cd0d18214fda961.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/e1ece15c11e14b8d8cd0d18214fda961"}}, "title": "Contribution of Rare Genetic Variation to Disease Susceptibility in a Large Scandinavian Myositis Cohort.", "authors": [{"family": "Bianchi", "given": "Matteo", "initials": "M", "orcid": "0000-0003-3394-6495", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3183e335a393486f8b6534db17b066d0.json"}}, {"family": "Kozyrev", "given": "Sergey V", "initials": "SV", "orcid": "0000-0001-6209-4100", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/cef7ddc40d8f47468f3f3dec3caa5de3.json"}}, {"family": "Notarnicola", "given": "Antonella", "initials": "A", "orcid": "0000-0003-0272-2931", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/708cd9cafb384ed29732f2c5fb1a17bd.json"}}, {"family": "Hultin Rosenberg", "given": "Lina", "initials": "L"}, {"family": "Karlsson", "given": "\u00c5sa", "initials": "\u00c5"}, {"family": "Pucholt", "given": "Pascal", "initials": "P", "orcid": "0000-0003-3342-1373", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b8d564c4e36f451f9b78f563c9e8fa07.json"}}, {"family": "Rothwell", "given": "Simon", "initials": "S", "orcid": "0000-0003-2123-9902", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6e28d139b79e4cf9a76140fd2ae830b3.json"}}, {"family": "Alexsson", "given": "Andrei", "initials": "A"}, {"family": "Sandling", "given": "Johanna K", "initials": "JK", "orcid": "0000-0003-1382-2321", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c5bbdb0cf40c48198ea04ede2fb33377.json"}}, {"family": "Andersson", "given": "Helena", "initials": "H"}, {"family": "Cooper", "given": "Robert G", "initials": "RG"}, {"family": "Padyukov", "given": "Leonid", "initials": "L", "orcid": "0000-0003-2950-5670", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/336dfd4ed41542338e3aae1e29ce1da2.json"}}, {"family": "Tj\u00e4rnlund", "given": "Anna", "initials": "A"}, {"family": "Dastmalchi", "given": "Maryam", "initials": "M"}, {"family": "ImmunoArray Development Consortium", "given": "", "initials": ""}, {"family": "DISSECT Consortium", "given": "", "initials": ""}, {"family": "Meadows", "given": "Jennifer R S", "initials": "JRS", "orcid": "0000-0002-0850-230X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9f363e8d74594ffeb0d68aa6d774b242.json"}}, {"family": "Pyndt Diederichsen", "given": "Louise", "initials": "L"}, {"family": "Molberg", "given": "\u00d8yvind", "initials": "\u00d8"}, {"family": "Chinoy", "given": "Hector", "initials": "H", "orcid": "0000-0001-6492-1288", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d3d7de322dd44925adf4ffdc01365f8f.json"}}, {"family": "Lamb", "given": "Janine A", "initials": "JA", "orcid": "0000-0002-7248-0539", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/07cd7a5b44b54240aa81d5f257743da4.json"}}, {"family": "R\u00f6nnblom", "given": "Lars", "initials": "L", "orcid": "0000-0001-9403-6503", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5f7ec7a7befd44cc988091ba0858d3c0.json"}}, {"family": "Lindblad-Toh", "given": "Kerstin", "initials": "K", "orcid": "0000-0001-8338-0253", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/612a779b69494f1ca9b6c5f1d84fd711.json"}}, {"family": "Lundberg", "given": "Ingrid E", "initials": "IE", "orcid": "0000-0002-6068-9212", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a2891140c49d446dbd82c96857bcde73.json"}}], "type": "journal article", "published": "2022-02-00", "journal": {"title": "Arthritis & rheumatology (Hoboken, N.J.)", "issn": "2326-5205", "volume": "74", "issue": "2", "pages": "342-352", "issn-l": "2326-5191"}, "abstract": "Idiopathic inflammatory myopathies (IIMs) are a heterogeneous group of complex autoimmune conditions characterized by inflammation in skeletal muscle and extramuscular compartments, and interferon (IFN) system activation. We undertook this study to examine the contribution of genetic variation to disease susceptibility and to identify novel avenues for research in IIMs.\n\nTargeted DNA sequencing was used to mine coding and potentially regulatory single nucleotide variants from ~1,900 immune-related genes in a Scandinavian case-control cohort of 454 IIM patients and 1,024 healthy controls. Gene-based aggregate testing, together with rare variant- and gene-level enrichment analyses, was implemented to explore genotype-phenotype relations.\n\nGene-based aggregate tests of all variants, including rare variants, identified IFI35 as a potential genetic risk locus for IIMs, suggesting a genetic signature of type I IFN pathway activation. Functional annotation of the IFI35 locus highlighted a regulatory network linked to the skeletal muscle-specific gene PTGES3L, as a potential candidate for IIM pathogenesis. Aggregate genetic associations with AGER and PSMB8 in the major histocompatibility complex locus were detected in the antisynthetase syndrome subgroup, which also showed a less marked genetic signature of the type I IFN pathway. Enrichment analyses indicated a burden of synonymous and noncoding rare variants in IIM patients, suggesting increased disease predisposition associated with these classes of rare variants.\n\nOur study suggests the contribution of rare genetic variation to disease susceptibility in IIM and specific patient subgroups, and pinpoints genetic associations consistent with previous findings by gene expression profiling. These features highlight genetic profiles that are potentially relevant to disease pathogenesis.", "doi": "10.1002/art.41929", "pmid": "34279065", "labels": [], "xrefs": [], "notes": [], "created": "2026-09-23T12:01:09.322Z", "modified": "2026-09-23T12:01:09.576Z"}]}