Purpose of review: The spondyloarthropathies (SpAs) are a group of interrelated inflammatory disorders with overlapping clinical features. Current SpA treatments only provide partial symptomatic and functional relief in a subgroup of patients. Consequently, there is a need to better understand the pathophysiology of SpA to develop more specific and effective treatments for these conditions.
Recent findings: Genetic and mechanistic evidence links SpA with inflammatory bowel disease (IBD) and psoriasis, and the symptoms of these diseases partially overlap. Regulatory T cells (Tregs) and dendritic cells control the adaptive immune response, and failures in their functions are likely to contribute to the establishment of chronic inflammation. The contributions of Tregs and dendritic cells to IBD and SpA have been assessed in both animal models of disease and patients.
Summary: Although defects in Tregs are important in psoriasis and in animal models of IBD, there is little evidence that they are important in SpA. However, data from animal models indicate that dendritic cells drive pathogenic T-cell responses, partly through the production of interleukin-23 (IL-23). Dendritic cells from SpA patients may also contribute to disease by producing IL-23, therefore supporting the differentiation of the Th17 cells that contribute to inflammation. The driving forces in SpA pathophysiology are now becoming clear; these data may lead to the development of novel therapies to target SpA and related inflammatory disorders.