title: B1a cells play a pathogenic role in the development of autoimmune arthritis.
abstract: Dysregulated functions of B1 cells have been implicated in the disease progression of various autoimmune disorders, but it remains largely unclear whether B1 cells are involved in the pathogenesis of autoimmune arthritis. In this study, we found that peritoneal B1a cells underwent proliferation and migrated to the inflamed joint tissue with upregulated RANKL expression during collagen-induced arthritis (CIA) development in mice. Adoptive transfer of B1a cells exacerbated arthritic severity and joint damage while intraperitoneal depletion of B1 cells ameliorated both arthritic symptoms and joint pathology in CIA mice. In culture, RANKL-expressing B1a cells significantly promoted the expansion of osteoclasts derived from bone marrow cells, which were in accord with the in vivo findings of increased osteoclastogenesis in CIA mice transferred with B1a cells. Together, these results have demonstrated a pathogenic role of B1a cells in the development of autoimmune arthritis through RANKL-mediated osteoclastogenesis.
authors.affiliation: Department of Pathology and Center of Infection and Immunology, The University of Hong Kong, Hong Kong, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Deng
authors.affiliation: Department of Pathology and Center of Infection and Immunology, The University of Hong Kong, Hong Kong, China.
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Pathology and Center of Infection and Immunology, The University of Hong Kong, Hong Kong, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Chen
authors.affiliation: Department of Rheumatology and Immunology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu, China.
authors.forename: Xiaoxuan
authors.initials: X
authors.lastname: Sun
authors.affiliation: Department of Pathology and Center of Infection and Immunology, The University of Hong Kong, Hong Kong, China.
authors.forename: Fan
authors.initials: F
authors.lastname: Xiao
authors.affiliation: Department of Pathology and Center of Infection and Immunology, The University of Hong Kong, Hong Kong, China.
authors.forename: King-Hung
authors.initials: KH
authors.lastname: Ko
authors.affiliation: Department of Rheumatology and Immunology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu, China.
authors.forename: Miaojia
authors.initials: M
authors.lastname: Zhang
authors.affiliation: Department of Pathology and Center of Infection and Immunology, The University of Hong Kong, Hong Kong, China.
authors.forename: Liwei
authors.initials: L
authors.lastname: Lu
mesh_terms: D000818:Animals; D001169:Arthritis, Experimental / Q000276:immunology* / Q000473:pathology; D001327:Autoimmune Diseases / Q000276:immunology* / Q000473:pathology; D001402:B-Lymphocytes / Q000276:immunology*; D001854:Bone Marrow Cells / Q000276:immunology; D002455:Cell Division / Q000276:immunology; D002465:Cell Movement / Q000276:immunology*; D049109:Cell Proliferation; D018450:Disease Progression; D005434:Flow Cytometry; D020297:Mice, Congenic; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D010010:Osteoclasts / Q000276:immunology; D010012:Osteogenesis / Q000276:immunology; D053245:RANK Ligand / Q000276:immunology / Q000378:metabolism
chemical_list: D053245:RANK Ligand; C505689:Tnfsf11 protein, mouse
keywords: B1 cell; Immune response; Immunity; Immunology and Microbiology Section; autoimmune disease; collagen-induced arthritis; receptor activator of nuclear factor kappa-B ligand