Objectives. Bone destruction is a remarkable feature of inflammatory arthritis. It remains unknown why arthritis associated with the systemic autoimmune/inflammatory condition systemic lupus erythematosus (SLE) does not result in erosion and destruction. We aimed to determine the role of autoantibody in the pathogenesis of non-erosive arthritis in SLE. Methods. We analysed medical record of SLE patients, investigated whether autoantibody induces arthritis lacking bone destruction in animal models and determined whether SLE autoantibody inhibits osteoclastogenesis induced by RANKL in vitro experiments. Results. We found that arthritis lacking bone erosions is common in SLE patients and lupus-prone mice. Intraarticular injection of lupus serum or IgG induces immune complex deposition and arthritis, but does not result in bone destruction. Deposition of IgG, monocytes/macrophages and TNF-a is all required for the development of arthritis. Lupus serum or IgG inhibits RANKLinduced differentiation of monocytes into osteoclast in a dosedependent manner. FccR acts as co-receptors for RANKL and is involved in osteoclastogenesis. Deficiency of FccRII or FccRIII does not affect osteoclastogenesis in the presence of SLE IgG. However, lupus IgG competes for FccRI binding with RANKL, thereby reducing osteoclastogenesis. Conclusion. Observations from this study demonstrate that IgG from SLE patients can induce arthritis and inhibits RANKL-induced osteoclastogenesis through competitive occupation of FccRI on monocytes/macrophages. This study improves the understanding of the pathophysiology of SLEassociated arthritis and offers a protective mechanism (FccRI inhibition) that may be targeted in other forms of autoimmune/ inflammatory arthritis, such as RA, to prevent or limit bone erosion and inflammatory bone loss.

Pulmonary arterial hypertension (PAH) is a group of devastating and progressive disorders, resulting in relentless increases in pulmonary vascular resistance. The number of studies related to PAH has been increasing in recent years. Our study aims to illustrate trends in PAH research over the past decade using bibliometric analysis. Science Citation Index-Expanded was adopted to search studies concerning PAH between 2011 and 2020. The bibliographic information was converted and analyzed automatically using a bibliometric package in R software and citespace. The annual quantity of publications on PAH showed an overall increase last decade. The United States was the most prolific country with 2,479 publications, and it was also the country that cooperated most with other countries. Hôpital Bicêtre made important research achievements on PAH and was a leader in study cooperation. Marc Humbert led the PAH field by publishing 150 articles in the past decade. During the past decade, there was a close transnational relation among countries or regions, institutions and authors. Further, Circulation was the most cited journal, followed by the Journal of the American College of Cardiology and the American Journal of Respiratory and Critical Care Medicine , with 3,895, 3,406, and 3,170 citations, respectively. The global research status and trend of PAH are deeply understood for the first time using bibliometric and visual methods, and the results of our study bring us a valuable reference for clinical researchers.

Bone erosion is one of the primary features of inflammatory arthritis and is caused by excessive differentiation and activation of osteoclasts. Fc gamma receptors (FcγRs) have been implicated in osteoclastogenesis. Our recent studies demonstrate that joint-deposited lupus IgG inhibited RANKL-induced osteoclastogenesis. FcγRI is required for RANKL-induced osteoclastogenesis and lupus IgG-induced signaling transduction. We reviewed the results of studies that analyzed the association between FcγRs and bone erosion in inflammatory arthritis. The analysis revealed the dual roles of FcγRs in bone destruction in inflammatory arthritis. Thus, IgG/FcγR signaling molecules may serve as potential therapeutic targets against bone erosion.