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A retrospective cohort study provides further insight into the 6-month outcomes of children with MIS-C, highlighting the importance of physical and mental rehabilitation.
The results of the AURORA 1 study show a superior effect on renal remission for voclosporin plus standard care over standard care alone in patients with lupus nephritis.
Results of a new study implicate tenascin C in entheseal new bone formation in ankylosing spondylitis and suggest this protein could be targeted therapeutically.
Targeting DNA methylation using a repurposed cancer drug reduces joint damage in mouse models of autoimmune arthritis by restoring the balance between T cell subsets.
According to new data, overexpression of the nicotinamide adenine dinucleotide (NAD) hydrolase, CD38, in systemic sclerosis (SSc) leads to NAD depletion and fibrosis. These intriguing findings link inflammation, NAD metabolism and fibrosis and bare striking resemblance to age-related changes in SSc. Could DNA damage also connect these seemingly unrelated pathways?
The transcription factor Sox9 is important for cartilage formation during development, but its role in postnatal growth plates and adult articular cartilage has been uncertain. New research is revealing essential roles for Sox9 in postnatal cartilage homeostasis and in preventing post-traumatic osteoarthritis, along with new mechanisms for chondrocyte-to-osteoblast transition.
The discovery that autoantibodies and other factors can predict the future onset of rheumatoid arthritis (RA) has encouraged the development of clinical trials looking at RA prevention. Although an exciting area of research, finding an approach that results in the successful completion of an RA prevention trial is challenging.
Ankylosing spondylitis (AS) is a chronic inflammatory disease with hallmarks of both autoimmune and autoinflammatory pathology. In this Review, the authors examine the evidence for both disease processes and aim to reconcile the two.
Monogenic autoinflammatory diseases are linked to various germline and somatic pathogenic variants but numerous factors must be considered to explain their large phenotypic variability. This Review discusses genotype–phenotype relationships and the potential molecular mechanisms that might explain this variability.
The intervertebral disc (IVD) is a hypoxic environment, and the hypoxia-inducible factor (HIF) family of transcription factors enable cells of the disc to adapt to these conditions. Understanding HIF-related mechanisms could help in the generation of therapies for IVD degeneration.
