Reviews & Analysis

Reactive arthritis is a form of inflammatory arthritis associated with bacterial infection. In this article, the authors describe the current state of our knowledge regardingChlamydia-induced reactive arthritis, including chlamydial persistence in joints, susceptibility factors and host and pathogen biology, and discuss future research priorities in this disease.

Increasing evidence suggests that extracellular DNA plays a part in the pathogenesis of systemic lupus erythematosus (SLE) independently of the involvement of anti-DNA autoantibodies. In this Perspectives article, the authors discuss the findings that have led to this conclusion, and explore the new therapeutic avenues that this discovery has opened. Specifically, the interesting prospect of targeting treatments at the structural manipulation of extracellular DNA is introduced and the strategies for achieving this goal that have shown promise in animal studies are presented.

Juvenile systemic sclerosis (JSSc) is a relatively rare disease compared to its adult equivalent. As a result, much of our knowledge of the disease is derived from studies in adult. Our understanding of JSSc has improved over the past 5 years, but considerable challenges remain in determining the optimal diagnostic and therapeutic protocols in these patients.

Autoantibodies, produced by autoreactive B cells, are involved in the pathology of rheumatic diseases including systemic lupus erythematosus (SLE). Modulation of B-cell function by inhibiting cytokines active on B cells or even eliminating B-cell populations can effectively treat SLE and other diseases. So far so simple, yet—as explored in this Perspective—the relationships between the effects of such therapies on B cells, the levels of individual autoantibodies, and clinical outcomes are fiendishly complex. Better knowledge of B-cell biology is needed to understand the effects of agents that target B cells, and to increase their efficacy.

A vast quantity of individual-level molecular data, including gene expression and genetic variation data, has become available in the past decade. Sirota and Butte discuss how integrative computational strategies can be applied to analyze this data across different rheumatic and autoimmune disorders. They outline the implications of such analyses, and discuss the current challenges and future directions of these approaches.

When two similar, credible analyses of the same patient database report seemingly contrasting risk estimates for the association with cancer of a widely-prescribed therapy, it is difficult for clinicians, never mind for patients, to make decisions about treatment options. Nevertheless, clinicians can—and must—interpret the available evidence for their patients, helping them to weigh the potential benefits and harms of their prescription.

Autoimmune-like syndromes (AILS), such as lupus-like syndrome and inflammatory neuropathies, are occasionally seen in patients treated with tumor necrosis factor (TNF) antagonists, although the pathogenetic mechanisms underlying these syndromes are not well understood. In this article, the author suggests that infections might trigger, amplify or mimic AILS in patients receiving anti-TNF therapy.

The disparity in the occurrence of rheumatoid arthritis (RA) between men and women is well documented, but the reasons for this difference remain poorly understood. In this article, the authors discuss the factors that might explain the sexual dimorphism of RA, including genetic, endocrine and behavioral differences, and how improving our understanding of the influence of these factors might lead to the development of novel treatments for patients with this disease.