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In our May issue: articles on B cell checkpoints in rheumatic diseases, myeloid cells in fibrogenesis and systemic sclerosis, spontaneous dog osteoarthritis and inclusion body myositis.
Image of skin from a patient with dermatomyositis. Image supplied by Majid Zeidi, Kristen Chen and Victoria P. Werth, University of Pennsylvania School of Medicine.
The molecular mechanisms responsible for initiation and progression of osteoarthritis (OA) are incompletely understood. New data implicate cholesterol, its metabolites and the receptor RORα as catabolic drivers of OA-like disease in mice, but do these data identify new targets for treating patients with OA?
Sensing of cytosolic DNA by cyclic GMP–AMP synthase (cGAS) is central to the pathogenesis of a number of autoinflammatory syndromes and possibly some autoimmune diseases, such as systemic lupus erythematosus (SLE). Activation of cGAS signalling requires its deacetylation, so might aspirin have therapeutic potential to treat SLE by acetylating cGAS?
Inclusion body myositis (IBM) is a slowly progressive disease characterized by unique clinical and pathological features. This Review discusses the historical and clinical aspects of IBM and the mounting evidence arguing for the important pathogenic function of the immune system.
Osteoarthritis occurs spontaneously in pet dogs, which often share environmental and lifestyle risk-factors with their owners. This Review aims to stimulate cooperation between medical and veterinary research under the One Medicine initiative to improve the welfare of dogs and humans.
Myeloid cells come in many shapes and sizes and are central to inflammatory processes. This Review puts myeloid cells and their inflammatory functions into the context of fibrosis and their contribution to pathology in systemic sclerosis.
B cells contribute to the pathogenesis of many rheumatic diseases. Targeting immune checkpoints that control the activation and effector function of B cells represents a promising therapeutic avenue.