ArticleClinical & translational immunology2020
Lupus IgG deposition causes arthritis but inhibits bone destruction through competitive occupation of FcγRI and reduced RANKL signalling.
Article in Clinical & translational immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Fc Gamma Receptors as Regulators of Bone Destruction in Inflammatory Arthritis.Frontiers in immunology · 2021Pooled it
- IgG promotes TNF-α induced osteoclastogenesis by upregulating the expression of TNFR1 and the NF-κB signalling pathway.Clinical & translational immunology · 2025Article
- HFD aggravated the arthritis and atherosclerosis by altering the intestinal status and gut microbiota.Molecular medicine (Cambridge, Mass.) · 2024Article
- Inhibitory effect of hydroxychloroquine on glucocorticoid-induced osteoporosis in lupus therapy.Clinical & translational immunology · 2024Article
- Immunoglobulin G inhibits glucocorticoid-induced osteoporosis through occupation of FcγRI.iScience · 2023Article
- The role of organ-deposited IgG in the pathogenesis of multi-organ and tissue damage in systemic lupus erythematosus.Frontiers in immunology · 2022Review
- Amelioration of Lupus Serum-Induced Skin Inflammation in CD64-Deficient Mice.Frontiers in immunology · 2022Article
- The Potential Role of RP105 in Regulation of Inflammation and Osteoclastogenesis During Inflammatory Diseases.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesBone 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.
methodsWe 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
resultsWe 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-α is all required for the development of arthritis. Lupus serum or IgG inhibits RANKL-induced differentiation of monocytes into osteoclast in a dose-dependent manner. FcγR acts as co-receptors for RANKL and is involved in osteoclastogenesis. Deficiency of FcγRII or FcγRIII does not affect osteoclastogenesis in the presence of SLE IgG. However, lupus IgG competes for FcγRI binding with RANKL, thereby reducing osteoclastogenesis.
conclusionObservations from this study demonstrate that IgG from SLE patients can induce arthritis and inhibits RANKL-induced osteoclastogenesis through competitive occupation of FcγRI on monocytes/macrophages. This study improves the understanding of the pathophysiology of SLE-associated arthritis and offers a protective mechanism (FcγRI 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.
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