To assess the prevalence and factors associated with discordance between patient and physician global assessments (PaGA and PGA) of SLE disease activity over time, and explore residual patient-perceived burden during remission.

Pulmonary manifestations of CTDs are associated with morbidity and mortality. Early recognition through screening ensures appropriate monitoring and management. The aim of this audit was to define standards for pulmonary screening in CTDs and assess practice in UK tertiary paediatric rheumatology centres.

The neural mechanisms underlying salience network (SN) dysfunction in SLE remain unclear. This study applied a comprehensive multimodal approach to characterize SN abnormalities in SLE patients.

TNF is a central regulator of immune responses, inflammation and programmed cell death, and has an essential role in maintaining tissue and immune homeostasis. Abnormal TNF signalling is implicated in a broad spectrum of physiological and pathological processes, as exemplified by monogenic disorders arising from dysregulation of core components of the TNF pathway. These rare conditions encompass various autoinflammatory syndromes, immunodeficiencies, autoimmune diseases and neurodegenerative conditions, and offer unique insights into the molecular mechanisms driving pathology via TNF-mediated inflammation and cell death. Collectively, these diseases underscore the importance of tightly regulated TNF signalling for immune balance and illustrate how distinct molecular defects can produce overlapping clinical phenotypes. Variability in pathway integration and tissue-specific gene expression further shapes disease presentation, whereas disruption of post-translational modifications and cell-death regulators have emerged as central pathogenic mechanisms. Together, these insights highlight the need for precise genetic and mechanistic understanding to inform diagnosis and therapeutic strategies.

Erosive hand osteoarthritis is a painful and inflammatory disease without effective treatments. In this study we aimed to investigate the efficacy of transcutaneous auricular vagus nerve stimulation (taVNS) compared with sham stimulation in patients with inflammatory erosive hand osteoarthritis.

Dual blockade of IL-4 and IL-13 in atopic dermatitis (AD) has been associated with activation of the IL-23/IL-17 axis, potentially leading to paradoxical psoriasis and PsA-like presentation. However, the specific cytokine responsible for these reactions remains unclear. We report a case series of PsA-like presentation following treatment with tralokinumab, an anti-IL-13 monoclonal antibody used for AD.

H syndrome is a rare autosomal recessive disorder caused by mutations in SLC29A3, encoding the nucleoside transporter hENT3. Its heterogeneous clinical presentation often includes skin hyperpigmentation, systemic inflammation, endocrinopathies and sensorineural hearing loss. However, typical cutaneous signs may be absent, leading to diagnostic challenges. The objective was to describe a patient with H syndrome misdiagnosed until adulthood as having cryopyrin-associated periodic syndrome (CAPS), due to overlapping clinical and functional features.

To assess the prevalence of aortitis and aortic dilation at diagnosis, estimate the progression of aortic diameter over time, and identify predictors of incident aortic dilation development in patients with newly diagnosed GCA.

This study evaluated the classification utility of incorporating parotid gland US for juvenile Sjögren's disease (jSjD) by testing its role in a weighted scoring (WS) model and comparing it with the standard 2016 ACR/EULAR classic model (CM).

Elevated neutrophil-to-lymphocyte ratio (NLR) ≥ 2.95 has been linked to adverse outcomes in SSc. This study aimed to determine whether elevated NLR can signal disease onset, identify NLR threshold predictive of poor prognosis, and describe its longitudinal variations.

Due to their non-specific clinical presentation and low prevalence, diagnostic delays are common in Takayasu arteritis (TA) and childhood PAN (cPAN), and may result in preventable organ damage. However, data on specific factors contributing to diagnostic delay in paediatric vasculitis remain limited. Objectives were to identify clinical, demographic and laboratory predictors of diagnostic delay in children with TA or cPAN, and to determine the characteristics associated with a delay of >30 days.

Endosomal traffic governs various core processes that maintain immune homeostasis and self-tolerance, including receptor signalling, antigen processing, cytokine secretion and cellular metabolism. Traffic-regulated receptors - both intracellular and on the cell surface - modulate immune sensing of infection, nutrient availability and endogenous stress signals arising from cellular or tissue injury. In rheumatic diseases, such as systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis, systemic sclerosis, Sjögren syndrome and osteoarthritis, mounting evidence implicates disruptions in endosomal pathways as important drivers of disease onset and progression. Dysregulated endosomal trafficking contributes to type I interferon activation via signalling through Toll-like receptors, aberrant autoantigen presentation, and altered expression of metabolite transporters in immune cells and target organs. Endosome trafficking mediates autophagosome formation, the production of exosomes and the turnover of organelles, such as mitochondria that generate oxidative stress, thereby controlling chronic inflammation and connective tissue remodelling. Therefore, understanding the molecular architecture of endosomal recycling pathways and their integration with immune cell function can provide important insight into rheumatic diseases. Restoring trafficking fidelity - through modulation of RAB GTPases, endosomal Toll-like receptor signalling, metabolic reprogramming, autophagic flux and extracellular vesicle biology - represents a promising therapeutic strategy.

Autoimmune rheumatic diseases (AIRDs), such as rheumatoid arthritis and systemic lupus erythematosus, substantially affect quality of life, with viral infections increasingly recognized as potential but underappreciated triggers of worsening preexisting AIRD symptoms. Despite growing evidence that post-viral infections are associated with heightened autoimmune activity and disease flares, the precise mechanisms underlying the complex virus-autoimmune response remain poorly understood. As AIRD is most prevalent in women, hormonal factors might have a role in AIRD pathogenesis. Hormones can influence immune regulation, potentially affecting the risk and severity of viral-induced AIRD flares. Given the global rise of viral disease outbreaks with increasing evidence of viral persistence in AIRD pathology, this Review addresses a critical knowledge gap in understanding the immune crosstalk during viral-induced AIRD flares. We place an emphasis on emerging viruses and their potential role in AIRD flares, exploring mechanisms of immune dysregulation, chronic inflammation, molecular mimicry, viral persistence and emerging therapeutic strategies to mitigate virus-induced AIRD exacerbations. This Review is aimed at shedding light on the mechanisms by which emerging viruses promote AIRD flares, serving as a practical guide to improve clinical management and therapeutic innovations.

We investigated whether gradual clinical changes in RA patients diagnosed over two decades contributed to their improving outcomes during follow-up.

The monocyte-to-high-density lipoprotein cholesterol ratio (MHR) is an emerging biomarker associated with inflammation and oxidative stress, being linked to cardiovascular events in patients with chronic kidney disease or those with diabetes. Given that monocyte activation plays a central role in the pathogenesis of thrombosis in APS, and that HDL-cholesterol suppresses monocyte activation, we aimed to investigate whether MHR could serve as a predictor for recurrent thrombotic events in APS patients.

To compare the clinical efficacy and safety of biological disease-modifying antirheumatic drugs (DMARDs) and Janus kinase(JAK) inhibitors in patients with early rheumatoid arthritis (RA).