{"entity": "journal", "iuid": "2649f2908134419c96a0cb6dbdcff10d", "timestamp": "2026-08-22T06:55:30.295Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/journal/Arthritis%20Res%20Ther.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/journal/Arthritis%20Res%20Ther"}}, "title": "Arthritis Res Ther", "issn": "1478-6362", "issn-l": null, "publications_count": 5, "publications": [{"entity": "publication", "iuid": "7e3556e6244c4305ab0a959c7f9c4118", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/7e3556e6244c4305ab0a959c7f9c4118.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/7e3556e6244c4305ab0a959c7f9c4118"}}, "title": "Correction: Longitudinal assessment of reactivity and affinity profile of anti-Jo1 autoantibodies to distinct HisRS domains and a splice variant in a cohort of patients with myositis and anti-synthetase syndrome.", "authors": [{"family": "Notarnicola", "given": "Antonella", "initials": "A"}, {"family": "Preger", "given": "Charlotta", "initials": "C"}, {"family": "Lundstr\u00f6m", "given": "Susanna L", "initials": "SL"}, {"family": "Renard", "given": "Nuria", "initials": "N"}, {"family": "Wigren", "given": "Edvard", "initials": "E"}, {"family": "Van Gompel", "given": "Eveline", "initials": "E"}, {"family": "Galindo-Feria", "given": "Angeles S", "initials": "AS"}, {"family": "Persson", "given": "Helena", "initials": "H"}, {"family": "Fathi", "given": "Maryam", "initials": "M"}, {"family": "Grunewald", "given": "Johan", "initials": "J"}, {"family": "Jakobsson", "given": "Per-Johan", "initials": "PJ"}, {"family": "Gr\u00e4slund", "given": "Susanne", "initials": "S"}, {"family": "Lundberg", "given": "Ingrid E", "initials": "IE"}, {"family": "Fernandes-Cerqueira", "given": "C\u00e1tia", "initials": "C"}], "type": "published erratum", "published": "2024-12-02", "journal": {"title": "Arthritis Res Ther", "issn": "1478-6362", "volume": "26", "issue": "1", "pages": "206", "issn-l": null}, "abstract": null, "doi": "10.1186/s13075-024-03446-y", "pmid": "39623418", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11610361"}, {"db": "pii", "key": "10.1186/s13075-024-03446-y"}], "notes": [], "created": "2026-08-21T12:40:48.260Z", "modified": "2026-08-21T12:40:48.290Z"}, {"entity": "publication", "iuid": "76bdf83c4c134942b9debdd80e493fe7", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/76bdf83c4c134942b9debdd80e493fe7.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/76bdf83c4c134942b9debdd80e493fe7"}}, "title": "Methotrexate promotes the release of granulocyte-macrophage colony-stimulating factor from rheumatoid arthritis fibroblast-like synoviocytes via autocrine interleukin-1 signaling.", "authors": [{"family": "Bergstr\u00f6m", "given": "Beatrice", "initials": "B"}, {"family": "Selld\u00e9n", "given": "Tilia", "initials": "T"}, {"family": "Bollmann", "given": "Miriam", "initials": "M"}, {"family": "Svensson", "given": "Mattias N D", "initials": "MND"}, {"family": "Ekwall", "given": "Anna-Karin Hultg\u00e5rd", "initials": "AH"}], "type": "journal article", "published": "2024-10-11", "journal": {"title": "Arthritis Res Ther", "issn": "1478-6362", "volume": "26", "issue": "1", "pages": "178", "issn-l": null}, "abstract": "Activated fibroblast-like synoviocytes (FLS) are drivers of synovitis and structural joint damage in rheumatoid arthritis (RA). Despite the use of disease-modifying drugs, only about 50% of RA patients reach remission in real-world settings. We used an unbiased approach to investigate the effects of standard-of-care methotrexate (MTX) and a Janus kinase inhibitor, tofacitinib (TOFA), on gene expression in RA-FLS, in order to identify untargeted disease mediators.\n\nPrimary RA-FLS were activated by stimulation with interleukin-1\u03b2 (IL-1\u03b2) or platelet-derived growth factor + IL-1\u03b2 in the presence or absence of MTX or TOFA, with or without additional inhibitors. Co-cultures of synovial cells were performed in direct and indirect systems. Cells were collected for RNA sequencing or qPCR, and supernatants were analyzed for protein concentrations.\n\nSix thousand three hundred fifty genes were differentially expressed, the majority being upregulated, in MTX-treated activated RA-FLS and 970 genes, the majority being downregulated, in TOFA-treated samples. Pathway analysis showed that MTX had largest effects on 'Molecular mechanisms of cancer' and TOFA on 'Interferon signaling'. Targeted analysis of disease-associated genes revealed that MTX increased the expression of cell cycle-regulating genes but also of pro-inflammatory mediators like IL-1\u03b1 (IL1A) and granulocyte-macrophage colony-stimulating factor, GM-CSF (CSF2). The MTX-promoted expression of CSF2 in activated RA-FLS peaked at 48 h, could be mediated via either NF-\u03baB or AP-1 transcription factors, and was abrogated by IL-1 inhibitors (IRAK4 inhibitor and anakinra). In a co-culture setting, MTX-treatment of activated RA-FLS induced IL1B expression in macrophages.\n\nMTX treatment induces secretion of IL-1 from activated RA-FLS which by autocrine signaling augments their release of GM-CSF. This unexpected effect of MTX might contribute to the persistence of synovitis.", "doi": "10.1186/s13075-024-03406-6", "pmid": "39394168", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11468154"}, {"db": "pii", "key": "10.1186/s13075-024-03406-6"}], "notes": [], "created": "2026-08-21T12:40:46.284Z", "modified": "2026-08-21T12:40:46.297Z"}, {"entity": "publication", "iuid": "17a7bfdfbfdd4e43a0241b4c4c38ac51", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/17a7bfdfbfdd4e43a0241b4c4c38ac51.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/17a7bfdfbfdd4e43a0241b4c4c38ac51"}}, "title": "Longitudinal assessment of reactivity and affinity profile of anti-Jo1 autoantibodies to distinct HisRS domains and a splice variant in a cohort of patients with myositis and anti-synthetase syndrome.", "authors": [{"family": "Notarnicola", "given": "Antonella", "initials": "A", "orcid": "0000-0003-0272-2931", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/708cd9cafb384ed29732f2c5fb1a17bd.json"}}, {"family": "Preger", "given": "Charlotta", "initials": "C"}, {"family": "Lundstr\u00f6m", "given": "Susanna L", "initials": "SL"}, {"family": "Renard", "given": "Nuria", "initials": "N"}, {"family": "Wigren", "given": "Edvard", "initials": "E"}, {"family": "Van Gompel", "given": "Eveline", "initials": "E"}, {"family": "Galindo-Feria", "given": "Angeles S", "initials": "AS"}, {"family": "Persson", "given": "Helena", "initials": "H"}, {"family": "Fathi", "given": "Maryam", "initials": "M"}, {"family": "Grunewald", "given": "Johan", "initials": "J"}, {"family": "Jakobsson", "given": "Per-Johan", "initials": "PJ"}, {"family": "Gr\u00e4slund", "given": "Susanne", "initials": "S"}, {"family": "Lundberg", "given": "Ingrid E", "initials": "IE"}, {"family": "Fernandes-Cerqueira", "given": "C\u00e1tia", "initials": "C"}], "type": "journal article", "published": "2022-03-02", "journal": {"title": "Arthritis Res Ther", "issn": "1478-6362", "volume": "24", "issue": "1", "pages": "62", "issn-l": null}, "abstract": "To address the reactivity and affinity against histidyl-transfer RNA synthetase (HisRS) autoantigen of anti-Jo1 autoantibodies from serum and bronchoalveolar lavage fluid (BALF) in patients with idiopathic inflammatory myopathies/anti-synthetase syndrome (IIM/ASSD). To investigate the associations between the reactivity profile and clinical data over time.\n\nSamples and clinical data were obtained from (i) 25 anti-Jo1+ patients (19 sera with 16 longitudinal samples and 6 BALF/matching sera at diagnosis), (ii) 29 anti-Jo1- patients (25 sera and 4 BALF/matching sera at diagnosis), and (iii) 27 age/gender-matched healthy controls (24 sera and 3 BALF/matching sera). Reactivity towards HisRS full-length (HisRS-FL), three HisRS domains (WHEP, antigen binding domain (ABD), and catalytic domain (CD)), and the HisRS splice variant (SV) was tested. Anti-Jo1 IgG reactivity was evaluated by ELISA and western blot using IgG purified from serum by affinity chromatography. In paired serum-BALF, anti-Jo1 IgG and IgA reactivity was analyzed by ELISA. Autoantibody affinity was measured by surface plasmon resonance using IgG purified from sera. Correlations between autoantibody reactivity and clinical data were evaluated at diagnosis and longitudinally.\n\nAnti-Jo1 IgG from serum and BALF bound HisRS-FL, WHEP, and SV with high reactivity at the time of diagnosis and recognized both conformation-dependent and conformation-independent HisRS epitopes. Anti-HisRS-FL IgG displayed high affinity early in the disease. At the time of IIM/ASSD diagnosis, the highest autoantibody levels against HisRS-FL were found in patients ever developing interstitial lung disease (ILD) and arthritis, but with less skin involvement. Moreover, the reactivity of anti-WHEP IgG in BALF correlated with poor pulmonary function. Levels of autoantibodies against HisRS-FL, HisRS domains, and HisRS splice variant generally decreased over time. With some exceptions, longitudinal anti-HisRS-FL antibody levels changed in line with ILD activity.\n\nHigh levels and high-affinity anti-Jo1 autoantibodies towards HisRS-FL were found early in disease in sera and BALF. In combination with the correlation of anti-HisRS-FL antibody levels with ILD and ILD activity in longitudinal samples as well as of anti-WHEP IgG in BALF with poor pulmonary function, this supports the previously raised hypothesis that the lung might have a role in the immune reaction in anti-Jo1-positive patients.", "doi": "10.1186/s13075-022-02745-6", "pmid": "35236390", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8889758"}, {"db": "pii", "key": "10.1186/s13075-022-02745-6"}], "notes": [], "created": "2026-08-21T12:40:43.939Z", "modified": "2026-08-21T12:40:44.012Z"}, {"entity": "publication", "iuid": "6976185254d94d34b0c6c41e6cd80778", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/6976185254d94d34b0c6c41e6cd80778.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/6976185254d94d34b0c6c41e6cd80778"}}, "title": "Two subgroups in systemic lupus erythematosus with features of antiphospholipid or Sj\u00f6gren's syndrome differ in molecular signatures and treatment perspectives.", "authors": [{"family": "Idborg", "given": "Helena", "initials": "H"}, {"family": "Zandian", "given": "Arash", "initials": "A"}, {"family": "Sandberg", "given": "Ann-Sofi", "initials": "AS"}, {"family": "Nilsson", "given": "Bo", "initials": "B"}, {"family": "Elvin", "given": "Kerstin", "initials": "K"}, {"family": "Truedsson", "given": "Lennart", "initials": "L"}, {"family": "Sohrabian", "given": "Azita", "initials": "A"}, {"family": "R\u00f6nnelid", "given": "Johan", "initials": "J"}, {"family": "Mo", "given": "John", "initials": "J"}, {"family": "Grosso", "given": "Giorgia", "initials": "G"}, {"family": "Kvarnstr\u00f6m", "given": "Marika", "initials": "M"}, {"family": "Gunnarsson", "given": "Iva", "initials": "I"}, {"family": "Lehti\u00f6", "given": "Janne", "initials": "J"}, {"family": "Nilsson", "given": "Peter", "initials": "P"}, {"family": "Svenungsson", "given": "Elisabet", "initials": "E"}, {"family": "Jakobsson", "given": "Per-Johan", "initials": "PJ"}], "type": "journal article", "published": "2019-02-18", "journal": {"title": "Arthritis Res Ther", "issn": "1478-6362", "volume": "21", "issue": "1", "pages": "62", "issn-l": null}, "abstract": "Previous studies and own clinical observations of patients with systemic lupus erythematosus (SLE) suggest that SLE harbors distinct immunophenotypes. This heterogeneity might result in differences in response to treatment in different subgroups and obstruct clinical trials. Our aim was to understand how SLE subgroups may differ regarding underlying pathophysiology and characteristic biomarkers.\n\nIn a cross-sectional study, including 378 well-characterized SLE patients and 316 individually matched population controls, we defined subgroups based on the patients' autoantibody profile at inclusion. We selected a core of an antiphospholipid syndrome-like SLE (aPL+ group; positive in the lupus anticoagulant (LA) test and negative for all three of SSA (Ro52 and Ro60) and SSB antibodies) and a Sj\u00f6gren's syndrome-like SLE (SSA/SSB+ group; positive for all three of SSA (Ro52 and Ro60) and SSB antibodies but negative in the LA test). We applied affinity-based proteomics, targeting 281 proteins, together with well-established clinical biomarkers and complementary immunoassays to explore the difference between the two predefined SLE subgroups.\n\nThe aPL+ group comprised 66 and the SSA/SSB+ group 63 patients. The protein with the highest prediction power (receiver operating characteristic (ROC) area under the curve = 0.89) for separating the aPL+ and SSA/SSB+ SLE subgroups was integrin beta-1 (ITGB1), with higher levels present in the SSA/SSB+ subgroup. Proteins with the lowest p values comparing the two SLE subgroups were ITGB1, SLC13A3, and CERS5. These three proteins, rheumatoid factor, and immunoglobulin G (IgG) were all increased in the SSA/SSB+ subgroup. This subgroup was also characterized by a possible activation of the interferon system as measured by high KRT7, TYK2, and ETV7 in plasma. In the aPL+ subgroup, complement activation was more pronounced together with several biomarkers associated with systemic inflammation (fibrinogen, \u03b1-1 antitrypsin, neutrophils, and triglycerides).\n\nOur observations indicate underlying pathogenic differences between the SSA/SSB+ and the aPL+ SLE subgroups, suggesting that the SSA/SSB+ subgroup may benefit from IFN-blocking therapies while the aPL+ subgroup is more likely to have an effect from drugs targeting the complement system. Stratifying SLE patients based on an autoantibody profile could be a way forward to understand underlying pathophysiology and to improve selection of patients for clinical trials of targeted treatments.", "doi": "10.1186/s13075-019-1836-8", "pmid": "30777133", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC6378708"}, {"db": "pii", "key": "10.1186/s13075-019-1836-8"}], "notes": [], "created": "2026-08-20T12:22:04.813Z", "modified": "2026-08-20T12:22:04.857Z"}, {"entity": "publication", "iuid": "7c1ae52d359c479285c7b7dfaaa42a40", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/7c1ae52d359c479285c7b7dfaaa42a40.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/7c1ae52d359c479285c7b7dfaaa42a40"}}, "title": "Cytokine production by activated plasmacytoid dendritic cells and natural killer cells is suppressed by an IRAK4 inhibitor.", "authors": [{"family": "Hjorton", "given": "Karin", "initials": "K", "orcid": "0000-0002-6211-3735", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a2ba2df9bec242ac8b67645001dc52a9.json"}}, {"family": "Hagberg", "given": "Niklas", "initials": "N"}, {"family": "Israelsson", "given": "Elisabeth", "initials": "E"}, {"family": "Jinton", "given": "Lisa", "initials": "L"}, {"family": "Berggren", "given": "Olof", "initials": "O"}, {"family": "Sandling", "given": "Johanna K", "initials": "JK"}, {"family": "Th\u00f6rn", "given": "Kristofer", "initials": "K"}, {"family": "Mo", "given": "John", "initials": "J"}, {"family": "DISSECT consortium", "given": "", "initials": ""}, {"family": "Eloranta", "given": "Maija-Leena", "initials": "ML"}, {"family": "R\u00f6nnblom", "given": "Lars", "initials": "L"}], "type": "journal article", "published": "2018-10-24", "journal": {"title": "Arthritis Res Ther", "issn": "1478-6362", "volume": "20", "issue": "1", "pages": "238", "issn-l": null}, "abstract": "In systemic lupus erythematosus (SLE), immune complexes (ICs) containing self-derived nucleic acids trigger the synthesis of proinflammatory cytokines by immune cells. We asked how an interleukin (IL)-1 receptor-associated kinase 4 small molecule inhibitor (IRAK4i) affects RNA-IC-induced cytokine production compared with hydroxychloroquine (HCQ).\n\nPlasmacytoid dendritic cells (pDCs) and natural killer (NK) cells were isolated from peripheral blood mononuclear cells (PBMCs) of healthy individuals. PBMCs from SLE patients and healthy individuals were depleted of monocytes. Cells were stimulated with RNA-containing IC (RNA-IC) in the presence or absence of IRAK4i I92 or HCQ, and cytokines were measured by immunoassay or flow cytometry. Transcriptome sequencing was performed on RNA-IC-stimulated pDCs from healthy individuals to assess the effect of IRAK4i and HCQ.\n\nIn healthy individuals, RNA-IC induced interferon (IFN)-\u03b1, tumor necrosis factor (TNF)-\u03b1, IL-6, IL-8, IFN-\u03b3, macrophage inflammatory protein (MIP)1-\u03b1, and MIP1-\u03b2 production in pDC and NK cell cocultures. IFN-\u03b1 production was selective for pDCs, whereas both pDCs and NK cells produced TNF-\u03b1. IRAK4i reduced the pDC and NK cell-derived cytokine production by 74-95%. HCQ interfered with cytokine production in pDCs but not in NK cells. In monocyte-depleted PBMCs, IRAK4i blocked cytokine production more efficiently than HCQ. Following RNA-IC activation of pDCs, 975 differentially expressed genes were observed (false discovery rate (FDR) < 0.05), with many connected to cytokine pathways, cell regulation, and apoptosis. IRAK4i altered the expression of a larger number of RNA-IC-induced genes than did HCQ (492 versus 65 genes).\n\nThe IRAK4i I92 exhibits a broader inhibitory effect than HCQ on proinflammatory pathways triggered by RNA-IC, suggesting IRAK4 inhibition as a therapeutic option in SLE.", "doi": "10.1186/s13075-018-1702-0", "pmid": "30355354", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC6235225"}, {"db": "pii", "key": "10.1186/s13075-018-1702-0"}], "notes": [], "created": "2026-08-21T12:40:41.763Z", "modified": "2026-08-21T12:40:41.840Z"}], "created": "2026-08-20T12:22:04.821Z", "modified": "2026-08-20T12:22:04.821Z"}