The past decade has seen many successes in translational rheumatology, from dramatic improvements in outcomes brought about by novel biologic therapies, to the discovery of new monogenic inflammatory disorders. Advances in molecular medicine, combined with progress towards precision care, provide an excellent opportunity to accelerate the translation of biological understanding to the bedside. However, although the field of rheumatology is a leader in the standardization of data collection and measures of disease activity, it lags behind in standardization of biological sample collection and assay performance. Uniform approaches are necessary for robust collaborative research, particularly in rare diseases. Standardization is also critical to increase reproducibility between centres, a prerequisite for clinical implementation of translational research. This Perspectives article emphasizes the need for standardization and implementation of best practices, presented in the context of lessons learned from international biorepository networks.

In diarthrodial joints, the articular cartilage, calcified cartilage, and subchondral cortical and trabecular bone form a biocomposite - referred to as the osteochondral unit - that is uniquely adapted to the transfer of load. During the evolution of the osteoarthritic process the compositions, functional properties, and structures of these tissues undergo marked alterations. Although pathological processes might selectively target a single joint tissue, ultimately all of the components of the osteochondral unit will be affected because of their intimate association, and thus the biological and physical crosstalk among them is of great importance. The development of targeted therapies against the osteoarthritic processes in cartilage or bone will, therefore, require an understanding of the state of these joint tissues at the time of the intervention. Importantly, these interventions will not be successful unless they are applied at the early stages of disease before considerable structural and functional alterations occur in the osteochondral unit. This Review describes the changes that occur in bone and cartilage during the osteoarthritic process, and highlights strategies for how this knowledge could be applied to develop new therapeutic interventions for osteoarthritis.

Adalimumab, an anti-TNF monoclonal antibody used to treat rheumatoid arthritis and other autoimmune disorders, paradoxically enhances the capacity of TNF to expand TNF receptor type II-expressing regulatory T cells. This provocative finding opens a new avenue for exploring the mechanisms that underlie efficacy, non-responsiveness and adverse effects associated with therapeutic targeting of TNF signalling.

Many rheumatic diseases are characterized by having an autoimmune background. Determining the mechanisms underlying autoimmunity is, therefore, important to further understand these diseases and to inform future lines of research aimed at developing new treatments and cures. As fast responders, innate lymphocytes have protective or pathogenic roles in the initiation as well as the maintenance of immune responses in general, and they contribute to tissue homeostasis, among other functions. Innate lymphocytes also seem to be involved in autoimmunity in particular. Since 2010, accumulating evidence clearly shows that different populations of innate lymphocytes have roles in responding to antigen-specific autoantibody and autoreactive T cells, thereby amplifying or attenuating disease processes. Cytotoxicity is a cardinal feature of many innate lymphocytes and can contribute to inflammatory tissue damage. Finally, innate lymphocytes can respond to biologic therapies for autoimmune diseases. Consequently, like TNF and other effector molecules, certain innate lymphocyte subsets might be appropriate therapeutic targets to ameliorate various autoimmune diseases. In this Review, we summarize the main characteristics and functions of innate lymphocyte subsets, and describe their roles in autoimmune disease. We also discuss how biologic therapies influence innate lymphocyte function and consider the potential for these cell subsets to act as future therapeutic targets.

Behçet's disease (BD), an auto-inflammatory vasculitis with oro-genital ulcerations, skin lesions and uveitis, is regarded as T cell mediated. A successful trial with rituximab suggests an additive role for B cells in the pathogenesis. Therefore, we studied B cell abnormalities in BD patients and the effect of TNF-blocking therapy.

The overexpression of IL-12 family cytokines is implicated in the pathogenesis of SSc, but their exact role is still unclear. The aim of this study was to investigate the regulation of extracellular matrix expression by IL-23 and its contribution to the phenotype of SSc.

Data on the relationship between disc degeneration (DD) and fragility fractures in men are limited. The aim of this study was to prospectively analyse the risk of vertebral and non-vertebral fractures in men with thoracolumbar DD according to the severity of its radiological signs: disc space narrowing (DSN), osteophytes and endplate sclerosis.

A national audit was performed assessing the early management of suspected inflammatory arthritis by English and Welsh rheumatology units. The aim of this audit was to measure the performance of rheumatology services against National Institute for Health and Care Excellence (NICE) quality standards (QSs) for the management of early inflammatory arthritis benchmarked to regional and national comparators for the first time in the UK.

Our aim was to conduct a national audit assessing the impact and experience of early management of inflammatory arthritis by English and Welsh rheumatology units. The audit enables rheumatology services to measure for the first time their performance, patient outcomes and experience, benchmarked to regional and national comparators.