B1a cells play a pathogenic role in the development of autoimmune arthritis

Oncotarget. 2016 Apr 12;7(15):19299-311. doi: 10.18632/oncotarget.8244.


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.

Keywords: B1 cell; Immune response; Immunity; Immunology and Microbiology Section; autoimmune disease; collagen-induced arthritis; receptor activator of nuclear factor kappa-B ligand.

MeSH terms

  • Animals
  • Arthritis, Experimental / immunology*
  • Arthritis, Experimental / pathology
  • Autoimmune Diseases / immunology*
  • Autoimmune Diseases / pathology
  • B-Lymphocytes / immunology*
  • Bone Marrow Cells / immunology
  • Cell Division / immunology
  • Cell Movement / immunology*
  • Cell Proliferation*
  • Disease Progression
  • Flow Cytometry
  • Mice, Congenic
  • Mice, Inbred C57BL
  • Mice, Inbred DBA
  • Osteoclasts / immunology
  • Osteogenesis / immunology
  • RANK Ligand / immunology
  • RANK Ligand / metabolism


  • RANK Ligand
  • Tnfsf11 protein, mouse