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).

Juvenile idiopathic arthritis (JIA) is the most prevalent chronic rheumatic disease in children, primarily affecting the joints but also influencing various organ systems, including the endocrine system. The interplay between JIA and endocrine dysfunctions remains an area of growing interest, as autoimmune and inflammatory mechanisms may contribute to the development of comorbid conditions. This review explores genetic markers associated with both JIA and endocrine disorders, the role of immune system dysregulation, and the impact of disease-modifying therapies on hormonal function. Additionally, the effects of chronic inflammation on endocrine homeostasis and metabolic regulation are discussed. Particular attention is given to conditions such as type 1 diabetes, Hashimoto's thyroiditis, and Cushing's syndrome, which may either precede JIA, arise as complications, or be exacerbated by its treatment. Effective JIA management requires an understanding of these mechanisms and a multidisciplinary approach.

Previous research has explored the uncertain association between metabolic syndrome (MetS) and bone mineral density (BMD). The objective of this study was to determine the prevalence of MetS in postmenopausal Moroccan women with osteoporosis and to examine the relationship between MetS, BMD, and bone turnover markers among this sample.

Behçet's disease (BD) presents with highly variable clinical manifestations and a heterogeneous pattern of symptom development. This study aimed to assess the chronology of symptom onset and clinical findings in BD patients at a nationally recognized Behçet's referral center and to examine associations between symptom progression and patient- and disease-related characteristics.

Biological treatments are indicated in familial Mediterranean fever (FMF) patients with colchicine resistance or intolerance. Interleukin-1 (IL-1) inhibitors may not yield sufficient efficacy and safety. Interleukin-6 inhibitors (tocilizumab - TCZ) have been suggested to be potentially beneficial. This systematic literature review aimed to evaluate the existing data on the efficacy and safety of IL-6 inhibitors in the treatment of FMF.

Biologic treatments have demonstrated increasing benefits for cardiovascular health in patients with rheumatoid arthritis (RA), including reductions in myocardial infarction risk factors, atherosclerosis progression, and the incidence of heart failure. This study aimed to compare treatment options: one combination of tumor necrosis factor inhibitors (adalimumab, etanercept) with methotrexate (MTX) and second treatment with anti-interleukin-6 (tocilizumab) - to determine whether cardiovascular effects are driven primarily by disease activity reduction or through distinct effects based on the mechanism of action. Moreover, we aimed to assess the influence of treatment on heart structure.

This study aimed to evaluate the readability, quality, reliability, similarity, and length of texts generated by ChatGPT on common rheumatic diseases and compare their content with American College of Rheumatology (ACR) patient education fact sheets.

Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare disorder characterized by eosinophil-rich inflammation and systemic necrotizing vasculitis affecting small to medium-sized vessels. The pathogenesis of EGPA is complex, involving both eosinophilic and vasculitic mechanisms, which contribute to a wide array of clinical manifestations. Treatment strategies primarily focus on immunosuppression, including glucocorticosteroids and biologic agents targeting eosinophils, to manage the diverse manifestations and improve patient outcomes. The authors reviewed the MEDLINE and PubMed databases to provide an updated overview of the pathogenetic mechanisms and current therapeutic strategies for the management of EGPA. We emphasize the diverse pathogenetic mechanisms underlying EGPA, focusing on both eosinophilic and vasculitic phenotypes. Additionally, we highlight contemporary therapeutic strategies, particularly the use of biologic agents targeting eosinophils, which represent a significant advancement in the management of the disease.

This study evaluated the efficacy and safety of anifrolumab (ANF) in patients with systemic lupus erythematosus (SLE) presenting with severe manifestations such as neuropsychiatric SLE (neuro-SLE), lupus nephritis, and antiphospholipid syndrome-associated SLE (APS-SLE), based on real-world clinical practice at a single center in Poland. This study is a retrospective analysis of patients with severe SLE who failed to achieve remission following previous immunosuppressive treatment and were subsequently started on ANF therapy.

Non-adherence to medicine results in poor disease control and increased morbidity. We determined the prevalence of treatment adherence and its associated factors in Kurdish patients with rheumatoid arthritis (RA) in Kurdistan Region. Disease severity was classified as mild (20%), moderate (46%), and severe (35%). Of the patients, 53% had other chronic diseases. Fifty-four percent always took their medications, 27% most of the time, and 17% sometimes. The study found that 38% experienced some side effects and found managing the medication schedule easy (52%) or very easy (34%). The patients reported that 30% missed a dose of medication, with the frequency of missed doses being rare (60%), occasional (16%), or frequent (24%). Sixty percent had regular access to medications. The barriers were the cost (78%) and availability of medications (27%), and side effects were reported to be significant barriers to adherence (26%). This study showed that the RA patients had high adherence to the treatment, with a high satisfaction rate.

Individuals with clinically suspect arthralgia (CSA, EULAR definition) are at increased risk of developing rheumatoid arthritis (RA) and early therapeutic intervention may delay or prevent progression. However, improved identification of likely progressors is needed to avoid unnecessary treatment. CD4+CXCR5+PD-1hi follicular helper (Tfh) and CD4+CXCR5-PD-1hi peripheral helper (Tph) T cells are implicated in RA pathogenesis. Notably, Tfh associate with favourable responses to co-stimulation blockade. Profiling these subsets in CSA could enhance our understanding of the RA preclinical phase, help identify progressors and select targeted therapies. Our objective was to assess circulating Tfh (cTfh) and Tph (cTph) cell frequencies in CSA.

Polymyalgia rheumatica (PMR) is the second most frequent inflammatory rheumatic disease in older adults, after rheumatoid arthritis. Recommendations for the management of PMR, developed by the German, Austrian and Swiss societies of rheumatology and other organizations were published in 2018.

Inflammatory arthritis refers to a group of related clinical entities marked mainly by inflammation of the joints, the spine, or both. Rheumatoid arthritis and spondyloarthritis (which includes psoriatic arthritis and axial spondyloarthritis) are the most common forms of inflammatory arthritis. As more studies are conducted, there are accumulating data suggesting the elevated risk of skin cancer, including both melanoma and non-melanoma skin cancer, in inflammatory arthritis compared with the general population. In this context, the question of whether screening for skin cancer should be recommended in individuals with inflammatory arthritis is more relevant than ever. In this Review, we discuss the current knowledge on the risk and possible associations of melanoma and non-melanoma skin cancer in inflammatory arthritis with the aim of raising awareness within the rheumatology community about the risk of skin cancer, screening, and guidance.