Annals of the Rheumatic Diseases最新文献

{"title":"Pseudogout, chondrocalcinosis, CPPD et al: crystal clear… or clear as mud?-The time has come to reconsider the nomenclature of calcium pyrophosphate deposition.","authors":"Silvia Sirotti, Charlotte Jauffret, Antonella Adinolfi, Edoardo Cipolletta, Daniele Cirillo, Luca Ingrao, Alessandro Lucia, Emilio Filippucci, Tristan Pascart, Sara K Tedeschi, Robert Terkeltaub, Nicola Dalbeth, Georgios Filippou","doi":"10.1016/j.ard.2025.04.004","DOIUrl":"10.1016/j.ard.2025.04.004","url":null,"abstract":"<p><p>Scientific interest in calcium pyrophosphate deposition (CPPD) has been limited by several challenges. These include difficulties in diagnosis due to diverse clinical presentations, the lack of classification criteria, the absence of standardised diagnostic modalities, underrecognition in clinical care, and, most significantly, the lack of evidence-based treatments. Consequently, CPPD was often regarded as the 'poor cousin' of gout. Fortunately, in recent years, CPPD has garnered increased attention from the rheumatology community. Milestones such as the first American College of Rheumatology/European Alliance of Association for Rheumatology classification criteria, the European Alliance of Association for Rheumatology recommendations for the use of imaging in clinical practice, validated OMERACT ultrasound definitions and scoring system, and the OMERACT core domain sets for CPPD have significantly advanced the field. Yet, unresolved issues regarding CPPD nomenclature hold back advancement in both research and clinical practice. The terminology surrounding CPPD remains inconsistent in the scientific literature, with numerous terms and acronyms used to describe the condition and its manifestations. For example, many 'pseudosyndromes' (eg, pseudogout) and purely radiographic descriptors (eg, chondrocalcinosis) are still commonly used by clinicians and researchers interchangeably, as either the name of the condition or one of its clinical or radiographic manifestations. This lack of standardisation complicates communication among health care professionals, researchers, and between doctors and patients, creating insurmountable barriers to effective care and research advances. In this viewpoint, we highlight the value of standardised terminology, drawing parallels with other rheumatic diseases. We aimed to explore the historical evolution of CPPD nomenclature, assess the impact of previous standardisation efforts, and propose a possible way for a common language.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1287-1292"},"PeriodicalIF":20.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Radiographic structural damage in axial spondyloarthritis: is there a preferred way to quantify progression over time? Comparison of blinded versus unblinded mSASSS scoring.","authors":"Xenofon Baraliakos, Mikhail Protopopov, Valeria Rios Rodriguez, Murat Torgutalp, Ani Dilbaryan, Hildrun Haibel, Joachim Sieper, Juergen Braun, Martin Rudwaleit, Denis Poddubnyy","doi":"10.1016/j.ard.2025.03.017","DOIUrl":"10.1016/j.ard.2025.03.017","url":null,"abstract":"<p><strong>Objectives: </strong>Structural progression in spine in axial spondyloarthritis (axSpA) is assessed by conventional radiographs and quantified by the modified Stoke Ankylosing Spondylitis Spine Score (mSASSS). Blinded mSASSS scoring might be associated with 'background noise,' and for assessing a slow-progressing disease such as axSpA, high sensitivity to change without loss of specificity is crucial. The aim of this study was to compare the sensitivity to change of blinded vs unblinded application of mSASSS for identification of a preferred way of assessing radiographic damage in axSpA over time.</p><p><strong>Methods: </strong>Cervical and lumbar radiographcs of axSpA patients participating in a national inception cohort (GErman SPondyloarthritis Inception Cohort) obtained at baseline and after 2 years were scored using the mSASSS by 5 experienced readers, 2 blinded and 3 unblinded to chronology. Mean scores were used for calculations.</p><p><strong>Results: </strong>Overall, 210 patients (37.3 years, 51% male, 79% human leukocyte antigen B27 positive) were included. The mean baseline mSASSS was 4.2 ± 8.3 vs 3.4±7.9 and mean mSASSS progression was 0.7 ± 2.3 vs 1.0 ± 1.9 for the blinded vs unblinded scoring method, respectively (P = .005). Progression of ≥2 mSASSS units was found in 30 (14.3%) vs 37 (17.6%) patients in blinded and unblinded scoring. In the shift analysis, mSASSS worsening was found in 35 (0.8%) vs 109 (2.2%) and improvement in 4 (0.1%) vs 2 (0.04%) of a total of 4.373 and 4914 vertebral edges in the blinded vs unblinded group, respectively. The majority of progression was found for the development of syndesmophytes in both groups.</p><p><strong>Conclusions: </strong>More mSASSS progression was detected using unblinded vs blinded scoring. Scoring spinal radiographs with known chronological order seems to be more sensitive to changes.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1335-1341"},"PeriodicalIF":20.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A cross-sectional observational study of patients with sicca with salivary autoantibodies defines a potential new phenotype of Sjögren's disease.","authors":"Martha Tsaliki, Joshua Cavett, Biji T Kurien, Christina Bruxvoort, Valerie M Lewis, John A Ice, Devavrat Dave, Sina Khosravani, Kiely Grundahl, Christopher J Lessard, Astrid Rasmussen, Kathy L Sivils, Amy Darise Farris, Kristi A Koelsch, Robert Hal Scofield","doi":"10.1016/j.ard.2025.03.012","DOIUrl":"10.1016/j.ard.2025.03.012","url":null,"abstract":"<p><strong>Objectives: </strong>Diagnosis of Sjögren's disease (SjD) consists of clinical examinations that include invasive studies such as lower lip biopsies and blood collection to identify presence of serum autoantibodies. Salivary glands of patients with SjD are sites where antibody-secreting cells accumulate and secrete immunoglobulins. Many patients with dry manifestations who do not meet classification criteria are grouped as non-Sjögren's sicca (NSS) and are heavily understudied. We undertook this cross-sectional observational study to investigate the role of salivary autoantibodies as a diagnostic tool and determine presence of salivary autoantibodies in patients with NSS.</p><p><strong>Methods: </strong>In this cross-sectional observational study, we screened whole unstimulated saliva from 446 subjects by direct enzyme-linked immunosorbent assays and capillary western blotting for anti-Ro60, anti-La, and rheumatoid factor (immunoglobulin (Ig)G and IgA) antibodies. All subjects were classified following the ACR/EULAR classification at the Oklahoma Medical Research Foundation Sjögren's Research Clinic.</p><p><strong>Results: </strong>Patients with SjD were significantly more likely to have salivary antibodies compared with those with NSS and healthy control subjects. In this cohort, there were 88 subjects with NSS with seronegative profiles who had detectable salivary autoantibodies and objective measures of dryness.</p><p><strong>Conclusions: </strong>Of these 88 subjects with NSS, we identified 75 subjects that had positive objective examinations of dryness and could belong to an early-onset SjD group. Alternatively, these 75 subjects with NSS could belong to a distinct phenotype of SjD that will remain seronegative while being saliva positive for anti-Ro60. These data showed a relationship between ocular and oral dryness and the presence of salivary anti-Ro60 antibodies in subjects with NSS.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1354-1362"},"PeriodicalIF":20.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adalimumab serum concentration to choose a subsequent biological DMARD in patients with rheumatoid arthritis (ADDORA-switch): results of a blinded randomised test-treatment trial.","authors":"Maike H M Wientjes, Sadaf Atiqi, Gerrit J Wolbink, Michael T Nurmohamed, Maarten Boers, Femke Hooijberg, Theo Rispens, Annick de Vries, Ronald F van Vollenhoven, Sofia Ramiro, Noortje van Herwaarden, Bart J F van den Bemt, Alfons A den Broeder","doi":"10.1016/j.ard.2025.03.015","DOIUrl":"10.1016/j.ard.2025.03.015","url":null,"abstract":"<p><strong>Objectives: </strong>A substantial proportion of patients with rheumatoid arthritis (RA) discontinue adalimumab due to ineffectiveness. The next treatment step can be another tumour necrosis factor inhibitor (TNFi) or a biological/targeted synthetic disease-modifying antirheumatic drug (b/tsDMARD). Therapeutic drug monitoring (TDM) of serum drug levels may help guide this choice. This study evaluated whether switching treatments based on adalimumab trough levels is more effective than random switching.</p><p><strong>Methods: </strong>In this 24-week, multicentre, triple-blinded, randomised controlled trial, patients with RA who stopped adalimumab due to inefficacy (disease activity score based on 28 joint count and C-reactive protein [DAS28-CRP] >2.9) were enrolled. Participants were randomly assigned (1:1) to a TDM-based or random switching (control) strategy. The primary outcome was the difference in mean time-weighted DAS28-CRP between groups at 24 weeks.</p><p><strong>Results: </strong>From July 2020 to November 2023, 83 consecutive patients with RA were included, with 78 initiating a new b/tsDMARD (TDM-based group: n = 38; control: n = 40). The mean time-weighted DAS28-CRP was 3.15 in both groups (TDM: SD, 0.99; control: SD, 1.01; 95% CI of difference: -0.46 to 0.47). There were no significant differences between the groups in flare rates, escape medication use, disease activity, or adverse events. Receiver operating characteristic analyses in the control group found no predictive value of adalimumab levels for response to TNFi or non-TNFi.</p><p><strong>Conclusions: </strong>Switching treatments based on adalimumab trough levels was not more effective than random switching in patients with RA who failed adalimumab treatment. Therefore, serum drug level measurements to guide therapy choices in this context is not recommended.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1293-1300"},"PeriodicalIF":20.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143954925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and validation of interferon-driven gene signature as a predictor of response to methotrexate in juvenile idiopathic arthritis.","authors":"Melissa Kartawinata, Wei-Yu Lin, Beth Jebson, Kathryn O'Brien, Elizabeth Ralph, Emma Welsh, Restuadi Restuadi, Elizabeth C Rosser, Claire T Deakin, Lucy R Wedderburn, Chris Wallace","doi":"10.1016/j.ard.2025.03.007","DOIUrl":"10.1016/j.ard.2025.03.007","url":null,"abstract":"<p><strong>Objectives: </strong>To identify and validate gene expression biomarkers of response to methotrexate (MTX) treatment in peripheral blood of children with juvenile idiopathic arthritis (JIA) measured before starting MTX treatment.</p><p><strong>Methods: </strong>RNA sequencing was performed on sorted CD4+, CD8+, CD14+, and CD19+ cells, as well as peripheral blood mononuclear cells (PBMC) taken pre-treatment in a discovery cohort (n = 97) and 2 validation cohorts (n = 26 and n = 47, respectively) of patients with non-systemic JIA. Clinical data were recorded at baseline (timepoint 1) prior to treatment and 6 months (timepoint 2) of MTX treatment. Analysis tested the association of gene expression in specific cell types with treatment response using limma-voom, gene set enrichment analysis, and a novel 51-gene score against response to treatment. Parallel analysis, also using pre-treatment gene expression data, was performed in adult rheumatoid arthritis (RA) data (n = 240).</p><p><strong>Results: </strong>In patients with JIA, the baseline expression of genes driven by interferon (IFN) alpha (type-I) or gamma (type-II) was associated with response to treatment at 6 months in 3 independent JIA cohorts. The direction of the association indicated that children with higher baseline expression of IFN-stimulated genes prior to MTX were more likely to be good responders. Comparison with adult RA indicated differences between PBMC and whole blood gene expression associations with response.</p><p><strong>Conclusions: </strong>In children with JIA, a high IFN-driven gene signature is associated with a better response to MTX than those with a low IFN-driven gene signature. These data could pave the way to clinically validated tools to identify those most likely to require medications in addition to MTX to control inflammation.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1412-1424"},"PeriodicalIF":20.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to the correspondence on \"CD19-CAR T-cell therapy induces deep tissue depletion of B cells\".","authors":"Carlo Tur, Markus Eckstein, Georg Schett, Maria Gabriella Raimondo","doi":"10.1016/j.ard.2025.03.006","DOIUrl":"10.1016/j.ard.2025.03.006","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"e38-e39"},"PeriodicalIF":20.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A coding single nucleotide polymorphism in the interleukin-6 receptor enhances IL-6 signalling in CD4 T cells and predicts treatment response to tocilizumab in giant cell arteritis.","authors":"Robert Zorc, Christopher Redmond, McKella Sylvester, Mary Maclean, Luciana Yamamoto de Almeida, Kaitlin A Quinn, Alessandro Tomelleri, Corrado Campochiaro, Lorenzo Dagna, Fernanda Gutierrez-Rodrigues, Kristina V Wells, Cameron Rankin, Sabrina Helmold Hait, Chloe Palmer, Robert Corty, Alexander Bick, Kathi Lambert, Jane H Buckner, John J O'Shea, Jin Kyun Park, Massimo Gadina, Peter C Grayson","doi":"10.1016/j.ard.2025.01.049","DOIUrl":"10.1016/j.ard.2025.01.049","url":null,"abstract":"<p><strong>Objectives: </strong>The study objective was to determine if a common single nucleotide polymorphism in the interleukin 6 (IL-6) receptor (rs2228145, p.Asp358Ala) predicted treatment response to tocilizumab in giant cell arteritis (GCA).</p><p><strong>Methods: </strong>Genetic sequencing of the rs2228145 locus was performed in 2 independent cohorts of patients with GCA. Peripheral blood mononuclear cells (PBMCs) from patients and controls were evaluated for expression of the interleukin 6 receptor (IL-6R) and its coreceptor, gp130, using flow cytometry. The same PBMCs were stimulated with IL-6 and evaluated for downstream targets of IL-6: STAT3 phosphorylation (pSTAT3) and IL-17A expression.</p><p><strong>Results: </strong>In total, 100 patients with GCA were included (derivation cohort n = 58; validation cohort n = 42). The rs2228145 variant predicted tocilizumab response in each cohort. In the derivation cohort, a gene dose-dependent response was observed with a 36% response rate in the homozygous patients and 95% response rate in patients without the variant (P = .003). In the validation cohort, tocilizumab response rates were 50% for homozygotes and 85% for patients without the variant (P = .04). pSTAT3 levels were significantly increased in response to IL-6 stimulation in a gene dose-dependent manner in CD4 T cells from patients with GCA but not controls. CD4 T cells from patients with GCA had significantly higher membrane expression of gp130 than healthy controls, and response to IL-6 correlated with gp130 expression. IL-17 producing CD4 T cells were increased in a gene dose-dependent response to IL-6 (P < .01).</p><p><strong>Conclusions: </strong>The rs2228145 variant is associated with decreased treatment response to tocilizumab and worse outcomes in GCA by enhancing CD4 T cell response to IL-6.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1401-1411"},"PeriodicalIF":20.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12313419/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143498077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Time-independent disease state identification defines distinct trajectories determined by localised vs systemic inflammation in patients with early rheumatoid arthritis.","authors":"Nils Steinz, Tjardo D Maarseveen, Erik B van den Akker, Andrew P Cope, John D Isaacs, Aaron R Winkler, Tom W J Huizinga, Yann Abraham, Rachel Knevel","doi":"10.1016/j.ard.2025.04.011","DOIUrl":"10.1016/j.ard.2025.04.011","url":null,"abstract":"<p><strong>Objectives: </strong>Patients with rheumatoid arthritis (RA) display different trajectories towards improvement of disease. We aimed to disentangle the heterogeneity of RA disease trajectories from the first clinical visit onwards using graph-based pseudotime analysis.</p><p><strong>Methods: </strong>We studied early patients with RA over 1.5 years in 2 data sets: Leiden (Netherlands), n = 1237, with 5017 visits, and Towards a Cure for Early Rheumatoid Arthritis (TACERA) (United Kingdom), n = 243, with 750 visits. We created a pipeline for time-independent clustering of clinical and haematologic features to identify disease states. Sequence analyses of these states defined the trajectories. We studied the predictability of the trajectories with baseline features.</p><p><strong>Results: </strong>Clustering identified 8 disease states with localised inflammation (joints) and systemic inflammation (erythrocyte sedimentation rate [ESR] or leucocytes) as the main discriminating factors. The disease state sequences consisted of 4 trajectories, which we independently replicated in TACERA: A, high ESR; B, rapid progression from many inflamed joints towards remission; C, high leucocytes; and D, many inflamed joints with poor prognosis. Systemic vs local inflammation patterns showed moderate predictability at baseline (sensitivity of 71% and precision of 0.73 for trajectory A, although lower precision of 0.52 for trajectory B), while other trajectories were less predictable. Trajectories C and D had strong resemblance with B at baseline but deteriorated into less favourable trajectories. Patients in trajectory A were more often female and on average older. The trajectories were not explained by time till disease-modifying antirheumatic drug, baseline disease activity, or symptom duration. The suboptimal trajectories coincided with worse patient-reported outcomes, even when the inflammation was mainly systemic.</p><p><strong>Conclusions: </strong>We identified 4 distinct trajectories in early RA, differentiating RA into localised vs systemic inflammation. Our results highlight potential differences in disease pathology and opportunities for further targeted treatment. Inevitably, patterns without linkage to our selected features could not be detected.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1301-1312"},"PeriodicalIF":20.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative exome sequencing and machine learning identify MICB and interferon pathway genes as contributors to SSc risk.","authors":"Shamika Ketkar, Hongzheng Dai, Lindsay Burrage, David Murdock, Brian Dawson, Marialbert Acosta-Herrera, Martin Kerick, Javier Martin, Kevin Wilhelm, Jennifer Kay Asmussen, Olivier Lichtarge, Regeneron Genetics Center, Shervin Assassi, Maureen D Mayes, Brendan H Lee","doi":"10.1016/j.ard.2025.05.009","DOIUrl":"10.1016/j.ard.2025.05.009","url":null,"abstract":"<p><strong>Objectives: </strong>Systemic sclerosis (SSc) is a complex autoimmune disease with both known and unidentified genetic contributors. While genome-wide association studies (GWAS) have implicated multiple loci, many reside in noncoding regions. We aimed to identify novel protein-coding variants and pathogenic pathways using exome sequencing (ES) integrated with an Evolutionary Action-Machine Learning (EAML) framework, single-cell RNA sequencing (scRNA-seq), and expression quantitative trait locus (eQTL) analysis.</p><p><strong>Methods: </strong>GWAS was conducted in 2,559 SSc cases and 893 controls of Caucasian ancestry, with replication in 9,846 cases and 18,333 controls of European ancestry. EAML prioritized genes with high-impact missense variants predictive of disease. Public scRNA-seq data from SSc and control skin biopsies were analyzed to localize gene expression across cell types. Whole blood eQTL data were used to identify regulatory effects of risk variants.</p><p><strong>Results: </strong>A novel SSc risk locus at MICB (rs2516497, P = 3.66 × 10^-13) was identified and replicated. EAML highlighted 284 genes enriched in interferon signaling. scRNA-seq localized MICB and NOTCH4 to fibroblasts and endothelial cells, while HLA class II genes were enriched in macrophages and fibroblasts. eQTL analysis confirmed regulatory effects at MICB, NOTCH4, and other prioritized genes, linking SSc-associated variants to transcriptional dysregulation.</p><p><strong>Conclusions: </strong>This integrative genomic study identifies novel risk loci and mechanistic pathways in SSc, highlighting MICB, NOTCH4, and interferon-related genes. The findings provide insight into the cellular and regulatory architecture of SSc and support the utility of combining ES, machine learning, scRNA-seq, and eQTL data in complex disease genetics.</p>","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"1363-1374"},"PeriodicalIF":20.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correspondence to: 'CD19-CAR T-cell therapy induces deep tissue depletion of B cells' by Tur et al.","authors":"Rahul K Patel, Chandra Mohan","doi":"10.1016/j.ard.2025.02.015","DOIUrl":"10.1016/j.ard.2025.02.015","url":null,"abstract":"","PeriodicalId":8087,"journal":{"name":"Annals of the Rheumatic Diseases","volume":" ","pages":"e36-e37"},"PeriodicalIF":20.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143690701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}