Giant cell arteritis (GCA) is a large vessel vasculitis characterized by granulomatous inflammation classically affecting the carotid artery branches. GCA most often presents with one or more classic clinical features which include headache, jaw claudication, temporal scalp tenderness, and polymyalgia rheumatica. In a minority of cases, GCA can adopt an "occult" presentation (i.e., failure to thrive in the setting of unexplained inflammation) where vascular manifestations affect vascular beds, such as lingual ulceration, not amenable to biopsy. While the diagnosis of GCA is often supported by temporal artery biopsy or imaging studies, such as temporal artery ultrasound or magnetic resonance angiography, these techniques are known to have limited sensitivity. As a result, there is the potential for GCA to be misdiagnosed where it presents both in the absence of classic clinical manifestations and without clear diagnostic evidence by imaging or histopathology.

Data regarding the relationship between socioeconomic status (SES) and incidence of Giant Cell Arteritis (GCA) is conflicting. No previous studies have explored whether SES influences the likelihood of undergoing temporal artery biopsy (TAB). The aim of this study was to determine whether SES influences access to TAB and rate of biopsy positivity in those with suspected GCA.

Once regarded as passive bystander cells of the tissue stroma, fibroblasts have emerged as active orchestrators of tissue homeostasis and disease. From regulating immunity and controlling tissue remodelling to governing cell growth and differentiation, fibroblasts assume myriad roles in guiding normal tissue development, maintenance and repair. By comparison, in chronic inflammatory diseases such as rheumatoid arthritis, fibroblasts recruit and sustain inflammatory leukocytes, become dominant producers of pro-inflammatory factors and catalyse tissue destruction. In other disease contexts, fibroblasts promote fibrosis and impair host control of cancer. Single-cell studies have uncovered striking transcriptional and functional heterogeneity exhibited by fibroblasts in both normal tissues and diseased tissues. In particular, advances in the understanding of fibroblast pathology in rheumatoid arthritis have shed light on pathogenic fibroblast states in other chronic diseases. The differentiation and activation of these fibroblast states is driven by diverse physical and chemical cues within the tissue microenvironment and by cell-intrinsic signalling and epigenetic mechanisms. These insights into fibroblast behaviour and regulation have illuminated therapeutic opportunities for the targeted deletion or modulation of pathogenic fibroblasts across many diseases.

Many monogenic autoinflammatory diseases, including DADA2 (deficiency of adenosine deaminase 2), HA20 (haploinsufficiency of A20), SAVI (STING-associated vasculopathy with onset in infancy), COPA syndrome, LAVLI (LYN kinase-associated vasculopathy and liver fibrosis) and VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome, present predominantly with vasculitis and constitute a substantial subgroup of vasculitic conditions associated with a 'probable aetiology'. The spectrum of monogenic vasculitis encompasses all sizes and types of blood vessel, ranging from large vessels to medium-size and small vessels, and from the arterial side to the venous side of the vasculature. Monogenic vasculitis typically starts early in life during infancy or childhood; VEXAS syndrome, which presents in late adulthood, is an exception. The activation of myeloid cells via inflammasome and nuclear factor-κB pathways, type I interferon-enhanced autoimmune mechanisms and/or dysregulated adaptive immune responses have an important role in the development of immune-mediated endothelial dysfunction and vascular damage. Genetic testing is essential for the diagnosis of underlying monogenic autoinflammatory diseases; however, the penetrance of genetic variants can vary. Increased awareness and recognition of distinctive clinical findings could facilitate earlier diagnosis and allow for more-targeted treatments.

To elucidate the prevailing concerns by analyzing the shifts in clinical profiles and therapeutic outcomes of patients with rheumatoid arthritis from 2003 to 2022, and offer guidelines to refine future treatment approaches.

Recent guidelines and recommendations for lupus nephritis (LN) suggest rapid glucocorticoid (GC) reduction; however, robust supporting evidence remains limited. This study aimed to evaluate the impact of rapid GC reduction on renal outcomes in patients with proliferative LN.

We aimed to assess the safety and efficacy of ultrasound-guided needle muscle biopsy (UGNMB) using a 14G biopsy needle in obtaining adequate samples for histological analysis and establishing an inflammatory idiopathic myopathy (IIM) diagnosis in patients with suspected myositis.

Osteoarthritis (OA) is a chronic disease primarily affecting older adults, mainly impacting the hip and knee joints. The increasing prevalence of OA contributes to rising healthcare demands and costs. Current OA treatment guidelines emphasize the importance of self-management education and guidance, particularly in promoting physical activity and weight management. In addition, improving sleep is crucial for managing OA. Developing effective self-management interventions necessitates a comprehensive understanding of the factors that facilitate these behaviors. Especially for changing health behaviors, it is important to focus on psychosocial factors. Therefore, this systematic review aimed to identify the psychosocial factors associated with physical activity, weight management, and sleep in adults with hip and/or knee OA.

Autoimmune rheumatic diseases are a heterogeneous group of conditions, including rheumatoid arthritis (RA) and systemic lupus erythematosus. With the increasing availability of large single-cell datasets, novel disease-associated cell types continue to be identified and characterized at multiple omics layers, for example, 'T peripheral helper' (TPH) (CXCR5- PD-1hi) cells in RA and systemic lupus erythematosus and MerTK+ myeloid cells in RA. Despite efforts to define disease-relevant cell atlases, the very definition of a 'cell type' or 'lineage' has proven controversial as higher resolution assays emerge. This Review explores the cell types and states involved in disease pathogenesis, with a focus on the shifting perspectives on immune and stromal cell taxonomy. These understandings of cell identity are closely related to the computational methods adopted for analysis, with implications for the interpretation of single-cell data. Understanding the underlying cellular architecture of disease is also crucial for therapeutic research as ambiguity hinders translation to the clinical setting. We discuss the implications of different frameworks for cell identity for disease treatment and the discovery of predictive biomarkers for stratified medicine - an unmet clinical need for autoimmune rheumatic diseases.

Dermatomyositis (DM) is an immune-mediated myopathy characterized by proximal muscle weakness, inflammation, and cutaneous manifestations. Up to 25% of DM patients have an associated malignancy. Those with cancer-associated DM often face worse prognoses, poorer treatment responses, and reduced survival rates. Interestingly, anti TIF1γ-positive DM patients are notably at increased risk for malignancy, yet the underlying mechanisms and clinical correlation remain poorly understood. Nailfold video capillaroscopy (NVC) is a safe, non-invasive method for assessing vascular abnormalities, previously explored in various DM subsets but not specifically in anti TIF1γ-positive DM patients with malignancy. This study aims to characterize NVC findings in anti-TIF1γ-positive DM and assess their clinical relevance, particularly in malignancy-associated cases.

Systemic vasculitis, common forms of which include anti-neutrophil cytoplasmic antibody-associated small-vessel vasculitis, large-vessel vasculitis and Behçet syndrome, are frequently complicated by arterial or venous thrombotic events (AVTEs). Newly identified entities such as DADA2 (deficiency of adenosine deaminase 2) and VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome, which are driven by genetic mutations, also exhibit vasculitic features and are associated with a high risk of AVTEs. AVTEs in systemic vasculitis, including monogenic forms of vasculitis, are due to the complex interaction of inflammation and coagulation. New insights into the pathogenetic mechanisms implicate endothelial dysfunction, immune complex deposition and the interplay of pro-inflammatory cytokines with prothrombotic factors, which collectively promote thrombus formation. AVTEs impose a substantial disease burden, complicate diagnosis and negatively affect prognosis by increasing the risk of morbidity and mortality. Early diagnosis and treatment are crucial to prevent lasting damage. Management strategies should target both thrombosis and underlying inflammation. Antithrombotic therapies, including low-dose aspirin, or oral anticoagulants should be used on the basis of individual thrombotic risk assessment. Immunosuppressive therapy is the cornerstone of treatment for arterial and venous thrombosis, particularly in Behçet syndrome, in which vascular inflammation has a crucial role in thrombotic complications.

In the TULIP-1 and TULIP-2 phase 3 trials, anifrolumab treatment was associated with clinical efficacy and clinically meaningful improvements in multiple patient-reported outcomes over 52 weeks in patients with moderate-to-severe systemic lupus erythematosus (SLE). At the end of TULIP-1 and TULIP-2 (week 52), eligible patients could reconsent to enter a 3-year long-term extension trial (TULIP-LTE). Here, we investigated changes in patient-reported outcomes during treatment with anifrolumab or placebo for up to 4 years in patients with SLE who were receiving standard therapy.

Considerable data support early treatment of rheumatoid arthritis (RA) to obtain disease remission. Data from the National Early Inflammatory Arthritis Audit (NEIAA) in England and Wales suggest that, despite recent improvements in referral-to-treatment times, remission rates remain unchanged. We investigated reasons for this disconnect by evaluating temporal trends, geographical variation, and predictors of remission in individuals with new RA diagnoses.

CD19-targeting chimeric antigen receptor (CAR) T-cell therapy has advanced treatment strategies for severe autoimmune diseases such as systemic lupus erythematosus (SLE), systemic sclerosis, and idiopathic inflammatory myopathy. Data regarding side-effects are mostly generated from patients with malignancies, but little is known about autoimmune disease-specific adverse events. This study aimed to describe autoimmune disease-specific adverse events that occur with CAR T-cell therapy.