Volume 12 Issue 7, July 2016

Type I interferon (IFN) is an attractive therapeutic target in systemic lupus erythematosus (SLE), a notion bolstered by the positive results of a recent clinical trial of the anti-IFN antibody sifalimumab in patients with SLE. Interestingly, sifalimumab worked best in patients with high expression of IFN-induced genes, supporting the idea that subgroups of patients might be targeted specifically.

Diagnostic algorithms for axial spondyloarthritis (SpA), and classification criteria for use in clinical trials, are being developed and refined. But can axial SpA be ruled out in young patients with only one clinical feature of SpA prior to imaging studies and HLA-B27 testing?

Non-radiographic axial spondyloarthritis (nr-axSpA) and radiographic axial spondyloarthritis (r-axSpA) are considered to be different spectra of the same disease. Accumulating data suggest a low transition rate from nr-axSpA to r-axSpA in patients with early disease and identify inflammation, smoking and HLA-B27 positivity as factors associated with transition.

Cases of systemic lupus erythematosus with onset during childhood seem to be more severe than adult-onset disease, possibly because of genetic influences. But is more-detailed information about the molecular heterogeneity of the disease needed in order to tailor treatments and improve prognosis?

In this article, the authors provide a comprehensive and timely review of the mechanisms and consequences of hypoxia in the biology of inflammatory arthritis, with a focus on mitochondrial function, hypoxia signalling pathways in rheumatoid arthritis, and therapeutic implications.

A growing body of evidence implicates the human gut microbiota in health and in disease, including spondyloarthritis, psoriatic arthritis and rheumatoid arthritis. This article explores the ways in which the microbiota influences innate and adaptive immune responses in the host.

Although changes associated with ageing promote the development of osteoarthritis (OA), ageing and OA are independent processes. In this Review, the authors discuss the mechanisms by which age-related factors contribute to OA through effects on articular cartilage and propose that future improvements in our understanding of these mechanisms will inform new therapies to slow or stop the progression of OA.

Besides their well-known role in cell death mechanisms, CD8⁺ T cells are now emerging as critical mediators of autoimmune diseases. CD8⁺T-cell homeostatic changes under inflammatory conditions, such as phenotypic variation and impaired regulation, provide insights into the pathogenesis of autoimmune arthritis and potential therapeutic targets.

A subset of lupus autoantibodies can penetrate nuclei and damage DNA in cells, with consequences for the pathophysiology of systemic lupus erythematosus as well as cancer risk. Noble et al. propose the lupus butterfly theory to explain the effects of these DNA-damaging lupus autoantibodies on the interplay between autoimmunity, DNA damage and cancer.