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Findings suggest that changes in serum IgG4 levels over time are predictive of IgG4-related disease relapse and might identify patients amenable to preventative treatment.
Two studies highlight the potential of inhibiting the transcription factor SIX1 or its downstream mediator plasminogen activator inhibitor 1 as a strategy to limit fibrosis in systemic sclerosis.
Drawing on my contrasting experiences as a patient in oncology and rheumatology, I have seen how the lack of precision-based diagnostics and meaningful endpoints limits progress in rheumatic disease. I believe biologically grounded classification systems and greater patient involvement are essential for more effective and responsive care.
The emergence of potent depletion therapies for the treatment of refractory autoimmunity has led to the concept of immune reset. Understanding whether immune reset equates to cure, and whether cure is achievable through non-depleting approaches, depends on the identification of immune biomarkers for measuring healthy and pathological immunity.
The findings of the pivotal RESET-RA trial demonstrate the clinical benefits and safety of an implanted neuromodulation device that stimulates the vagus nerve for the treatment of rheumatoid arthritis.
Comparing dermatomyositis with cutaneous lupus erythematosus, single-cell analysis identifies monocyte-mediated endothelial injury as a dermatomyositis-specific feature and highlights JAK1 inhibition as a potential therapeutic approach.
An erythrocyte-based strategy to achieve durable immunotolerance prevents the formation of neutralizing antibodies against uricase and facilitates urate clearance in animal models of gout.
A new study reveals that the Epstein–Barr virus can reprogramme autoreactive B cells into pathogenic antigen-presenting cells in systemic lupus erythematosus, providing a mechanistic link between infection and autoimmunity.
Autologous haematopoietic stem cell transplantation revolutionized the treatment of severe systemic sclerosis as the first therapy able to induce long-term remission in this relentlessly fibrosing disease. Nevertheless, questions remain about patient selection, conditioning, and how this treatment fits into the evolving immune-modifying therapeutic landscape. The field should move beyond standardization towards precision therapy.
A new study uncovers how UBA1 mutations in VEXAS syndrome simultaneously promote myeloid inflammatory cell death and skew haematopoietic stem cells towards a myeloid lineage.
The results of the phase II DAHLIAS trial support the development of the neonatal Fc receptor blocker nipocalimab for the treatment of Sjögren disease.
A new population-based study suggests that sodium–glucose cotransporter-2 (SGLT2) inhibitors — originally developed for glycaemic control — reduce the risk of autoimmune rheumatic diseases.
In a phase III placebo-controlled trial, the addition of telitacicept to standard therapy led to increased clinical response rates for people with systemic lupus erythematosus.
Biallelic loss-of-function mutations in PLD4, as identified in five patients with SLE, lead to Toll-like receptor-driven hyperactivation of type I interferon, immune cell expansion and autoimmunity.