Abstract
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by high levels of autoantibodies and multiorgan tissue damage [1]. Arthritis is common in patients with SLE [2]. Bone erosion is a remarkable feature in arthritis such as rheumatoid arthritis (RA), but they are usually absent in arthritis of SLE [3]. Thus, this is particularly striking for clinical doctors because synovial biopsies from SLE patients show similar synovial inflammation to those in RA [4].
Highlights
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by high levels of autoantibodies and multiorgan tissue damage [1]
Lupus IgG blocks RANKL-induced monocyte differentiation into osteoclasts that contribute to bone erosion, Fc RI exerts a critical role in pathogenesis of lupus arthritis lacking bone erosion [8]
In mouse model of arthritis induced by intraarticular injection of lupus IgG, the severity of arthritis was significantly reduced in mice with monocyte depletion but not affected in mice with lymphocyte deficiency and mice with neutrophil depletion [8]
Summary
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by high levels of autoantibodies and multiorgan tissue damage [1]. *Corresponding author: Guo Min Deng, Department of Rheumatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. Autoantibody IgG Protects Bone Erosion and Destruction in SLE Arthritis. It remains unknown whether and how joint deposited lupus IgG contributes to arthritis without bone erosions in SLE.
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