SUMMARYWe analysed 112 idiopathic inflammatory myopathy (IIM) sera for the presence of anti-Ro, anti-La and anti-histidyl-tRNA synthetase (Jo-1) autoantibodies, and subsequently mapped B cell epitopes on the Ro52 protein recognized by anti-Ro52 þ IIM sera. Sera were characterized by immunoblotting, ELISA and RNA precipitation. Both anti-Ro60 and anti-La activity was found in 4% of IIM sera. Anti-Ro52 antibodies were present in 20% of IIM sera. However, in anti-Jo-1 þ IIM sera (21%), the frequency of the anti-Ro52 antibodies was found to be much higher (58%). No cross-reactivity between anti-Ro52 and anti-Jo-1 antibodies could be detected in these sera. To learn more about the nature of anti-Ro52 antibodies occurring in IIM sera, we analysed the major epitopes of the Ro52 protein targeted by antiRo52 þ IIM sera by immunoprecipitation of in vitro translated Ro52 deletion mutants. The major epitope was mapped in the region bordered by amino acids 126 and 252. This part of the protein includes a long a-helical region which contains two potential coiled-coil domains as well as a leucine zipper motif. Although no difference in Ro52 epitope recognition between anti-Jo-1 þ and anti-Jo-1 ¹ IIM sera could be observed, our results suggest that the autoimmune response against Ro52 and Jo-1 in IIM patients is coupled.

BackgroundIn blinded trials, transitioning from an innovator to a biosimilar has shown to be equivalent to maintenance on innovator biologic treatment in rheumatic diseases. However, data on open label transitioning to a biosimilar are scarce. Recently, we sequentially implemented two biosimilar transition projects (from innovator infliximab (REM) to biosimilar infliximab (CT-P13) and from innovator etanercept (ENB) to biosimilar etanercept (SB4)) in patients with a rheumatic disease using different communication strategies.ObjectivesTo investigate the impact of different communication strategies on the acceptance and persistence rates after transitioning from ENB to SB4 in 2016 and transitioning from REM to CT-P13 in 2015.MethodsAdult patients treated with REM or ENB were informed by letter about the request to transition to a biosimilar. Subsequently, patients were approached by telephone to ask whether they agreed. After the transition of REM to CT-P13 had finished, communication was enhanced for the transition of ENB to SB4 by 1) informing all patients at the same time directly followed by a national media item, 2) reporting that lower costs and fewer injection site reactions (demonstrated in a previous trial) were the reason for transitioning, 3) providing a “soft skills” training for rheumatology and pharmacy staff about how to assuage patient concerns regarding a biosimilar and how to act if a patient has objective or subjective health complaints (discuss possible nocebo response and incorrect causal attribution). Also, group think effects did not play a role during SB4 treatment (individual subcutaneous versus group intravenous administration). Transitioning patients were eligible for inclusion in the BIO-SWITCH study (switch REM to CT-P13) and BIO-SPAN study (switch ENB to SB4)1. Demographic, disease and treatment specific characteristics at baseline and disease activity and adverse events (AEs) during 6 months follow-up were collected.Results196 of 222 (88%) REM-treated patients and 636 of 643 (99%) ENB-treated patients transitioned to respectively CT-P13 and SB4 (delta 11%, 95% CI 7% to 16%). Until January 1st 2017, 479 of 636 (75%) patients gave informed consent for the BIO-SPAN study. Baseline characteristics were similar, except for disease duration and innovator treatment duration (both shorter in the BIO-SPAN cohort; p<0.01). Drug survival of patients on SB4 was adjusted for confounders greater than patients on CT-P13 (Figure 1; adjusted Hazard Rate 0.21, 95% CI 0.13 to 0.34). During 84 person-years of follow-up 47 patients discontinued CT-P13 (56/100 person-years; 26% due to inefficacy, 74% due to AEs). In contrast, 36 patients discontinued SB4 during 230 person-years of follow-up (16/100 person-years; 53% due to inefficacy, 42% due to AEs and 5% due to remission).ConclusionsUse of an enhanced communication strategy, together with more experience and absence of group think effects, resulted in much higher acceptance and persistence rates after open label shared decision making biosimilar transitio...

Objective. The cartilage proteins melanoma inhibitory activity (MIA) and human cartilage gp-39 (HC gp-39) are candidate autoantigens in rheumatoid arthritis (RA). The present study was undertaken to investigate the endogenous HLA-DR4-restricted presentation of these self proteins, in order to seek in vivo evidence in support of their potential immunologic role. The mechanisms that cause and sustain rheumatoid arthritis (RA) remain poorly elucidated. The association of the disease with certain class II major histocompatibility complex (MHC) haplotypes, however, strongly suggests that specific antigens are presented by antigen-presenting cells (APCs) to CD4ϩ T lymphocytes (1,2). Previous studies indicate that cartilage could be the source of some of these antigens in RA (3-7). In the present study we investigated the local presence and presentation of 2 cartilage-derived proteins that have distinct properties: human cartilage gp-39 (HC gp-39) and a protein called melanoma inhibitory activity (MIA).

No predictive value of baseline adalimumab, etanercept and infliximab DL or ADAb for successful dose reduction or discontinuation in RA was found in this context, with the possible exception of high adalimumab trough levels for successful dose reduction.

Our results suggest that the WOMAC-PF is able to detect changes over time in physical function and therefore should be the measure of first choice in clinical trials evaluating the effectiveness of an intervention on physical function in knee OA patients.