Research Papers: Immunology:

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

Jun Deng _, Xiaohui Wang, Qian Chen, Xiaoxuan Sun, Fan Xiao, King-Hung Ko, Miaojia Zhang and Liwei Lu

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2016; 7:19299-19311. https://doi.org/10.18632/oncotarget.8244

Metrics: PDF 2498 views  |   HTML 3528 views  |   ?  


Jun Deng1, Xiaohui Wang1, Qian Chen1, Xiaoxuan Sun2, Fan Xiao1, King-Hung Ko1, Miaojia Zhang2 and Liwei Lu1

1 Department of Pathology and Center of Infection and Immunology, The University of Hong Kong, Hong Kong, China

2 Department of Rheumatology and Immunology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu, China

Correspondence to:

Liwei Lu, email:

Miaojia Zhang, email:

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

Received: November 29, 2015 Accepted: March 14, 2016 Published: March 21, 2016


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.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 8244