Arthritis Research & Therapy最新文献

{"title":"Site-level cutaneous phenotyping framework for anti-MDA5-positive dermatomyositis: exploratory associations with systemic immune reference markers.","authors":"Ziyuan Tian, Lingbo Bi, Jiahui Han, Ke Xue, Yong Cui","doi":"10.1186/s13075-026-03834-6","DOIUrl":"10.1186/s13075-026-03834-6","url":null,"abstract":"<p><strong>Objectives: </strong>To propose and evaluate a CDASI-informed, medical-record-based site-by-lesion cutaneous phenotyping framework for anti-MDA5-positive dermatomyositis, using established systemic and immunological markers as reference anchors to examine whether this framework provides additional phenotypic resolution beyond conventional binary skin assessment.</p><p><strong>Methods: </strong>This single-centre retrospective cross-sectional study enrolled 339 anti-MDA5-positive DM patients. Cutaneous involvement was coded as binary ulceration, itch, and scale features across seven prespecified anatomical regions. The framework was CDASI-informed but did not use formal CDASI activity or damage scores. FLATCAN components, PAH, IgG, and IgM were used as systemic and immunological reference markers. Analyses included FDR-corrected univariate screening, hypothesis-driven multivariable association models, restricted cubic spline analysis, exploratory internal model-performance summaries, cross-correlation SVD (CC-SVD), and exploratory clustering.</p><p><strong>Results: </strong>The framework revealed complementary skin-systemic association patterns. First, the spatial extent of ulceration refined a conventional binary ulcer signal: any cutaneous ulceration was associated with CD8 + T-cell depletion (OR = 3.35, P < 0.001; FDR q = 0.026), and ulcer site count remained independently associated with CD8 + depletion (OR = 1.43 per site, P = 0.008). Second, anatomical location contributed distinct information: facial ulceration was associated with PAH (OR = 2.28, P = 0.003) more strongly than overall ulcer site count. Third, lesion-feature type separated different immunological patterns, with ulceration preferentially associated with CD8+/IgG-related signals and itch with IgM-related signals. CC-SVD organised these observations into exploratory dimensions, including a bootstrap-stable facial involvement-PAH/infection dimension and a statistically less stable acral ulcer-CD8+/IgG dimension.</p><p><strong>Conclusion: </strong>Site-by-lesion cutaneous phenotyping may provide a useful framework for studying phenotypic heterogeneity in anti-MDA5-positive dermatomyositis. The observed associations are exploratory and require prospective validation using standardised skin assessment and clinical outcome follow-up.</p>","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13471506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148175178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytokine-induced PD-L1 and PD-L2 expression is preserved but reverse signalling is altered in rheumatoid arthritis fibroblast-like synoviocytes.","authors":"Tilia Selldén, Anna-Karin Hultgård Ekwall, Georgios Chatziagorou, Anna-Carin Lundell, Anna Rudin","doi":"10.1186/s13075-026-03841-7","DOIUrl":"10.1186/s13075-026-03841-7","url":null,"abstract":"<p><strong>Background: </strong>Dysfunctional programmed cell death-1 (PD1) signalling may contribute to persistent immune activation in rheumatoid arthritis (RA). However, co-inhibitory molecule interactions between T cells and fibroblast-like synoviocytes (FLS) remain insufficiently understood. This study aimed to determine whether T cell activation and subset-associated cytokines differentially regulate the expression of PD-ligand 1 (PD-L1) and PD-L2 on FLS from RA patients compared with non-inflammatory (NI) controls, and whether PD1 engagement induces distinct transcriptional downstream responses in RA-FLS versus NI-FLS.</p><p><strong>Methods: </strong>Primary FLS cell lines were cultured from synovial tissue of patients with established RA or NI controls undergoing arthroscopy due to previous injury. Cells were cultured with CD3+ T cells or stimulated with TNF, IFNγ, IL-4, or TGF-β, and PD-L1 and PD-L2 expression was analysed by flow cytometry. PD-L1 and PD-L2 knockout FLS were generated using CRISPR/Cas9. TNF-primed knockout or mock-transfected RA- and NI-FLS were treated with soluble PD1, and transcriptomic responses were analysed by total mRNA sequencing.</p><p><strong>Results: </strong>Analysis of publicly available RNA-sequencing datasets showed that, in early RA, PD-L1 and PD-L2 expression were significantly higher in lymphoid compared to myeloid and fibroid synovial tissue pathotypes. In established RA, PD-L1 and PD-L2 expression in FLS showed a trend towards higher levels in lymphocyte-rich compared to lymphocyte-poor tissue. In vitro, activated but not resting T cells upregulated both PD-L1 and PD-L2 on FLS. Further, TNF and IFNγ induced PD-L1 expression up to fourfold compared with unstimulated FLS, whereas IL-4 and TGF-β had no effect. PD-L2 was induced by TNF, IFNγ, and IL-4 to similar levels. PD-L1 and PD-L2 expression did not differ between RA- and NI-FLS either in co-culture with T cells or under cytokine stimulation. Finally, soluble PD1-induced reverse signalling in FLS altered the expression of threefold more genes in NI-FLS compared to RA-FLS, indicating that RA-FLS might be less responsive to PD1 signalling. PD-L1 or PD-L2 knockout further showed that reverse signalling through each ligand modulates distinct gene sets in FLS.</p><p><strong>Conclusions: </strong>Cytokine-induced PD-L1 and PD-L2 expression is preserved in FLS from established RA but PD1-ligand signalling is altered, potentially contributing to the loss of immune regulation in RA.</p>","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"28 1","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the SARM1-cADPR-Ca²⁺ pathway attenuates mitochondrial fragmentation and osteoarthritis progression.","authors":"Yu Gu, Xin-Hao Zhao, Bai-Zhou Xing, Biao Wu, Rong Peng, Chang-Qing Li, Hai Lv, Hua-Ding Lu","doi":"10.1186/s13075-026-03837-3","DOIUrl":"10.1186/s13075-026-03837-3","url":null,"abstract":"<p><strong>Introduction: </strong>Osteoarthritis (OA) is a prevalent degenerative joint disease accompanied by increased number of senescent chondrocytes. Mitochondrial dysfunction is a well-established hallmark of chondrocyte senescence in OA pathogenesis. Sterile α and Toll/Interleukin-1 Receptor motif-containing 1 (SARM1), known to drive mitochondrial impairment in various cell types, has not been thoroughly investigated in the context of chondrocyte aging or OA.</p><p><strong>Methods: </strong>We established a doxorubicin (DOX)-induced senescence model in primary mouse chondrocytes. Gain- and loss-of-function approaches were employed using siRNA-mediated knockdown and lentiviral overexpression of SARM1, followed by assessment of senescence markers, mitochondrial function, and morphology. To investigate the mechanistic pathway, exogenous cyclic ADP-ribose (cADPR) and its specific inhibitor 8-Br-cADPR were applied, with subsequent evaluation of intracellular calcium dynamics and Drp1 translocation to mitochondria. We next tested the efficacy of blocking this SARM1/cADPR axis both ex vivo on human femoral head tissue as well as in an experimental OA mouse model.</p><p><strong>Results: </strong>Chondrocytes isolated from human OA cartilage and aged murine cartilage showed increased expression of SARM1. Knockdown of SARM1 reduced DOX-induced chondrocyte senescence and mitochondrial dysfunction, while overexpression of wild-type but not catalytic-inactive SARM1-TIR domain mutant (TIR-E642A) induced intrinsic apoptosis and mitochondrial fragmentation. Exogenous cADPR recapitulated senescence and mitochondrial fragmentation, whereas treatment with 8-Br-cADPR abolished SARM1-dependent effects. Mechanistically, SARM1-generated cADPR increased intracellular calcium levels, triggering Drp1 phosphorylation at Ser616 and dephosphorylation at Ser637, thereby resulting in Drp1-FIS1 interaction and mitochondrial fission. Interestingly, pharmacological or genetic inhibition of the SARM1/cADPR pathway ameliorated cartilage degradation in the experimental OA model.</p><p><strong>Conclusion: </strong>We show that SARM1 mediates mitochondrial fragmentation by activating cADPR-dependent calcium signaling, which in turn promotes Drp1 binding to FIS1. This suggests an unappreciated role for the SARM1-cADPR pathway in OA etiology and presents this pathway as an attractive candidate to be targeted therapeutically.</p>","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deficiency of Krüppel-like factor 15 activates β-catenin and is involved in the development of osteoarthritis : Author.","authors":"Akira Saitoh, Shinya Hayashi, Toshiki Kitamura, Takuma Hayashi, Kohei Motono, Shotaro Araki, Takuma Maeda, Yoshihito Suda, Kensuke Wada, Kemmei Ikuta, Masanori Tsubosaka, Tomoyuki Kamenaga, Yuichi Kuroda, Naoki Nakano, Tomoyuki Matsumoto, Tetsuya Hosooka, Wataru Ogawa, Ryosuke Kuroda","doi":"10.1186/s13075-026-03838-2","DOIUrl":"10.1186/s13075-026-03838-2","url":null,"abstract":"<p><p>Krüppel-like factor 15 is a metabolism-related transcription factor that has been implicated in the regulation of the Wnt/β-catenin signaling pathway. This study aimed to elucidate its function in cartilage, particularly its interaction with β-catenin, using inducible cartilage-specific knockout mice. Krüppel-like factor 15 knockout mice and control mice underwent destabilization of medial meniscal surgery to induce osteoarthritis. Histological analysis and immunohistochemistry were carried out, along with in vitro co-immunoprecipitation, double immunofluorescence, and subcellular fractionation, and a dual-luciferase reporter assay. The effects of Wnt3A stimulation and treatment with Wnt/β-catenin inhibitors were evaluated. Knockout mice showed significantly more cartilage degeneration at eight weeks after surgery when compared with control mice. Knockout mice also showed elevated Osteoarthritis Research Society International scores and increased expression of β-catenin, matrix metalloprotease-13, and a disintegrin-like metalloprotease with thrombospondin motifs-5, along with decreased expression of SRY-box transcription factor 9. Krüppel-like factor 15 was seen to physically interact and colocalize with β-catenin in chondrocyte nuclei. Its deficiency promoted canonical Wnt/β-catenin pathway activation and nuclear β-catenin accumulation. Consistently, dual-luciferase reporter assays demonstrated increased β-catenin/TCF transcriptional activity in Krüppel-like factor 15-deficient chondrocytes, which was further enhanced by Wnt3A stimulation. Wnt3A stimulation amplified catabolic gene expression and suppressed anabolic factor expression. However, administration of a Wnt/β-catenin signaling inhibitor canceled out these effects. This study indicates that Krüppel-like factor 15 interacts with β-catenin and functions as a negative regulator of Wnt/β-catenin signaling in cartilage, maintaining matrix homeostasis, and suppressing osteoarthritis progression. Deficiency of Krüppel-like factor 15 promotes catabolism and inhibits anabolism mediated by β-catenin in cartilage. These findings suggest that Krüppel-like factor 15 may be a potential therapeutic target for osteoarthritis, either by restoring its function or enhancing its interaction with β-catenin.</p>","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13410871/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated ST2⁺ Tregs in RA-ILD: correlation with pulmonary fibrosis and the IL-33/ST2/AREG axis.","authors":"Peiyan Zhang, Jiawei Wang, Haoyang Sun, Jinlin Miao, Zhaohui Zheng","doi":"10.1186/s13075-026-03836-4","DOIUrl":"10.1186/s13075-026-03836-4","url":null,"abstract":"<p><strong>Background: </strong>Interstitial lung disease (ILD) represents a significant extra-articular complication associated with rheumatoid arthritis (RA), contributing substantially to the morbidity and mortality observed in affected patients. Despite its clinical relevance, the underlying mechanisms driving the pathogenesis of RA-ILD remain poorly understood, necessitating further investigation into the immunological factors that may play a role in this condition.</p><p><strong>Methods: </strong>This study aimed to elucidate the role of ST2⁺ regulatory T cells (Tregs) in the progression of RA-ILD. To achieve this, we developed a composite murine model that integrated collagen-induced arthritis (CIA) with intratracheal bleomycin (BLM) administration, thereby simulating the pathophysiological features of RA-ILD. Concurrently, using flow cytometric and artificial intelligence-based quantitative analysis of high-resolution computed tomography (HRCT), we analyzed a clinical cohort consisting of healthy controls, RA patients without ILD (RA-nonILD), and RA patients with ILD (RA-ILD).</p><p><strong>Results: </strong>Histopathological assessment confirmed that the composite model exhibited exacerbated lung inflammation and fibrosis. Notably, flow cytometry revealed a marked expansion of ST2⁺ Tregs in both the lungs of CIA + BLM mice and the peripheral blood of RA-ILD patients. Moreover, quantitative HRCT analysis indicated a positive correlation between the frequency of ST2⁺ Tregs and fibrotic lung volume in patients. RA-ILD patients exhibited elevated serum levels of IL-33 and amphiregulin (AREG), which correlated with disease severity. In vitro studies further demonstrated that IL-33 stimulation significantly upregulated AREG expression at both the mRNA and protein levels in Tregs.</p><p><strong>Conclusion: </strong>These results highlight the potential involvement of the IL-33/ST2 axis in mediating a pathogenic Tregs response characterized by AREG production, thereby linking systemic autoimmunity to the progression of lung fibrosis in RA-ILD. Importantly, this study identifies the IL-33/ST2/AREG axis and ST2⁺ Tregs as promising biomarkers and therapeutic targets for RA-ILD, laying the groundwork for future mechanistic studies and translational research endeavors.</p>","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13410587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating immune cell biomarkers in Psoriatic Arthritis: associations with clinical manifestations and treatment response in the TOFA-PREDICT trial.","authors":"F T Perton, J N Pouw, J Spierings, D N Kors, A N Concepcion, C P J Bekker, H E Vonkeman, S C Mooij, L G Schipper, A Herman, S A Vreugdenhil, S C Mastbergen, P M J Welsing","doi":"10.1186/s13075-026-03833-7","DOIUrl":"10.1186/s13075-026-03833-7","url":null,"abstract":"<p><strong>Background: </strong>To investigate the associations of circulating immune cell biomarkers with clinical manifestations and treatment response in Psoriatic Arthritis (PsA), and to evaluate whether these biomarkers improve prediction of individual response to tofacitinib, methotrexate, or etanercept.</p><p><strong>Methods: </strong>Data from the TOFA-PREDICT development cohort (n = 80) were used. DMARD naïve patients were randomized to tofacitinib or methotrexate, and csDMARD inadequate responders were randomized to tofacitinib or etanercept. Treatment response (achievement of Minimal Disease Activity) was scored at week 16. Clinical data and peripheral blood mononuclear cells were analyzed at baseline and week 16. Relevant biomarkers for clinical manifestations or treatment response were selected using sparse partial least squares (sPLS) regression and extreme gradient boosting. Associations with PsA clinical manifestations were analyzed using multivariate linear regression. Biomarker profiles for treatment response were derived by sPLS regression. Lastly, a Ridge regression model was used to evaluate whether selected biomarkers improved the prediction of individual treatment response beyond a previously developed clinical model.</p><p><strong>Results: </strong>The biomarkers explained up to 27% and 11% of observed variance for psoriasis severity and the swollen joint count, respectively. Baseline biomarker profiles classified etanercept and methotrexate responders relatively well, but did not distinguish tofacitinib responders. Adding biomarker data to clinical data did not improve the accuracy of individual response prediction (AUC-ROC 0.74).</p><p><strong>Conclusion: </strong>Our comprehensive set of circulating immune cell biomarkers showed no additional value in precision medicine, when added to clinical predictors. However, the observed associations provide relevant insights into pathophysiological mechanisms underlying differential treatment response and clinical manifestations.</p><p><strong>Trial registration: </strong>EudraCT Trial registration number 2017-003900-28, registration date January 25th 2018.</p>","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13397704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148040940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Integrated analysis of dermatomyositis reveals heterogeneous immune infiltration and interstitial lung disease-associated endotype.","authors":"Xinzhi Xu, Tianwen Qiu, Kexin Sun, Xue Han, Junxia Huang, Xiuyuan Wang, Jianchao Ge, Ji Yang","doi":"10.1186/s13075-026-03832-8","DOIUrl":"10.1186/s13075-026-03832-8","url":null,"abstract":"","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"28 1","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13214371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148026372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serological biomarkers of JIA-associated uveitis: ANA titers, ANA AC-30 staining pattern and prefoldin 5 antibodies.","authors":"Heinrike Schmeling, Jens Klotsche, Babatope O Adebiyi, Frank Dressler, Dirk Foell, Ivan Foeldvari, Johannes-Peter Haas, Arnd Heiligenhaus, Gerd Horneff, Anton Hospach, Tilmann Kallinich, Jasmin Kuemmerle-Deschner, Kirsten Moenkemoeller, Prasad T Oommen, Christiane Reiser, Frank Weller-Heinemann, Daniel Windschall, Marvin J Fritzler, Kirsten Minden","doi":"10.1186/s13075-026-03835-5","DOIUrl":"10.1186/s13075-026-03835-5","url":null,"abstract":"<p><strong>Objective: </strong>To identify serum biomarkers associated with the development of uveitis in a German juvenile idiopathic arthritis (JIA) cohort.</p><p><strong>Methods: </strong>A convenience sample, enriched for uveitis cases, was drawn from a prospectively followed inception cohort of newly diagnosed JIA patients (ICON). Baseline serum samples were biobanked, and each was tested for conventional and novel autoantibodies using multi-analyte array technologies. Associations between uveitis occurrence, disease outcomes, and autoantibody profiles were examined.</p><p><strong>Results: </strong>Fifty-two patients with and 141 patients without uveitis were included in the analyses. At first uveitis documentation, 26% of patients presented with uveitis-related complications. Younger age at JIA diagnosis, higher ANA titers (median [IQR]: 960 [240-5120] vs. 160 [0-640]; p < 0.001), and the Anti-Cell (AC-30) immunofluorescence (IIF) staining pattern (63.5% vs. 23.4%; p < 0.001) were significantly associated with the presence of uveitis, but not with uveitis-related complications. In contrast, the AC-4 IIF staining pattern was more often present in children without uveitis. In addition, patients with uveitis showed significantly higher prefoldin subunit 5 (PFDN5) antibody titers compared to non-uveitis JIA patients (mean ± SD; 486.39 ± 495.85 vs. 321.85 ± 330.36; p = 0.010). Other tested autoantibodies, including anti-histone antibodies, were rare in both groups and did not differ significantly.</p><p><strong>Conclusions: </strong>High ANA titers, the AC-30 ANA indirect immunofluorescence (IIF) pattern, and younger age at JIA onset are significantly associated with uveitis in JIA. Anti-PFDN5 antibodies show potential as a novel biomarker for JIA-associated uveitis. Combining these serological markers with clinical risk factors may improve early identification of high-risk patients and support the development of better tailored screening strategies to prevent vision-threatening complications.</p>","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13386789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148026296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Induction of cervical disc degeneration and discogenic pain by low concentration Propionibacterium acnes infection: an in vivo animal study.","authors":"Jie Li, Hui Li, Yilei Chen, Dikai Bei, Bao Huang, Kaifeng Gan, Peiming Sang, Junhui Liu, Zhi Shan, Jian Chen, Fengdong Zhao, Binhui Chen","doi":"10.1186/s13075-026-03824-8","DOIUrl":"10.1186/s13075-026-03824-8","url":null,"abstract":"","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"28 1","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13196023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148004390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Real-world sex differences in treatment persistence and reasons for discontinuation in psoriatic arthritis patients: results from the German RABBIT-SpA register.","authors":"Lisa Lindner, Anja Weiß, Andreas Reich, Christine Baumann, Frank Behrens, Xenofon Baraliakos, Anne C Regierer","doi":"10.1186/s13075-026-03820-y","DOIUrl":"10.1186/s13075-026-03820-y","url":null,"abstract":"","PeriodicalId":8419,"journal":{"name":"Arthritis Research & Therapy","volume":"28 1","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13191841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147986259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}