IFN α Kinoid (IFN-K) is a therapeutic vaccine composed of IFNα2b coupled to a carrier protein. In a phase I/II placebo-controlled trial, we observed that IFN-K significantly decreases the IFN gene signature in whole blood RNA samples from SLE patients. Here, we analysed extended follow-up data from IFN-K-treated patients, in order to evaluate persistence of neutralizing anti-IFNα Abs antibodies (Abs), and gene expression profiling.

The present study aimed to determine the protective effects of dietary supplementation with resveratrol (RSV) in an acute antigen-induced arthritis (AIA) model.

In clinical trials of RA, it is common to assess effectiveness using end points based upon dichotomized continuous measures of disease activity, which classify patients as responders or non-responders. Although dichotomization generally loses statistical power, there are good clinical reasons to use these end points; for example, to allow for patients receiving rescue therapy to be assigned as non-responders. We adopt a statistical technique called the augmented binary method to make better use of the information provided by these continuous measures and account for how close patients were to being responders.

Autophagy, an endogenous process necessary for the turnover of organelles, maintains cellular homeostasis and directs cell fate. Alterations to the regulation of autophagy contribute to the progression of various rheumatic diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), osteoarthritis (OA) and systemic sclerosis (SSc). Implicit in the progression of these diseases are cell-type-specific responses to surrounding factors that alter autophagy: chondrocytes within articular cartilage show decreased autophagy in OA, leading to rapid cell death and cartilage degeneration; fibroblasts from patients with SSc have restricted autophagy, similar to that seen in aged dermal fibroblasts; fibroblast-like synoviocytes from RA joints show altered autophagy, which contributes to synovial hyperplasia; and dysregulation of autophagy in haematopoietic lineage cells alters their function and maturation in SLE. Various upstream mechanisms also contribute to these diseases by regulating autophagy as part of their signalling cascades. In this Review, we discuss the links between autophagy, immune responses, fibrosis and cellular fates as they relate to pathologies associated with rheumatic diseases. Therapies in clinical use, and in preclinical or clinical development, are also discussed in relation to their effects on autophagy in rheumatic diseases.

ACPAs are associated with bone destruction in RA. The aim of this study was to evaluate the association between ACPA and bone destruction in patients with a distinct inflammatory disorder, PsA.

The aim of this study was to evaluate the course of SSc-related pulmonary abnormalities following high-dose chemotherapy with autologous stem cell transplantation (SCT) by quantitative chest CT analysis and compare the results with those of pulmonary function tests and the response of cutaneous involvement.

The aim was to investigate the importance of aspects of health for patients with axial SpA (axSpA) and to explore differences across different subgroups.

Comorbid medical conditions may influence treatment and contribute to poor outcomes in early RA. We aimed to assess the association of baseline comorbidity with outcomes in early inflammatory arthritis using data from the Canadian Early Arthritis Cohort.

Increased atherosclerosis in RA is not fully explained by the ordinary risk factors, but it may be related to vascular inflammation. The aim of this study was to investigate the degree of carotid artery inflammation in drug-naive patients with early RA before and after DMARD triple therapy.