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Pathogenic conversion of regulatory B10 cells into osteoclast-priming cells in rheumatoid arthritis.

Abstract：

:Regulatory B10 cells were functionally impaired in rheumatoid arthritis (RA), yet the mechanisms were unclear. B cells are recently recognized as important participants in osteoclastogenesis by producing RANKL. In this study, we investigated whether regulatory B10 cells could convert into RANKL-producing cells, thus impairing their immunosuppressive functions in RA and exacerbating the disease progression. Our results showed that human regulatory B10 cells could ectopically express RANKL. Under RA circumstance, RANKL-producing B10 cells expanded dramatically, partially induced by TNF-α. The frequencies of these cells were positively correlated with RA patient disease activities and tender joint counts, but negatively correlated with the frequencies of regulatory B10 cells. Strikingly, RANKL-producing B10 cells from RA patients, but not healthy individuals significantly promoted osteoclast differentiation and bone erosion in a paracrine and cell-cell contact-dependent manner. Moreover, these pathogenic RANKL-producing B10 cells declined while regulatory IL-10-producing B10 cells increased in RA patients with disease remission after therapy. Collectively, these results showed that in RA, regulatory B10 cells demonstrated the potential of converting into RANKL-producing cells, thus exacerbating osteoclast formation, bone destruction and disease progression. Modulating the status of B10 cells might provide novel therapeutic strategies for RA.

journal_name

J Autoimmun

journal_title

Journal of autoimmunity

authors

Hu F,Liu H,Liu X,Zhang X,Xu L,Zhu H,Li Y,Shi L,Ren L,Zhang J,Li Z,Jia Y

doi

10.1016/j.jaut.2016.09.002

subject

Has Abstract

pub_date

2017-01-01 00:00:00

pages

53-62

eissn

0896-8411

issn

1095-9157

pii

S0896-8411(16)30141-X

journal_volume

76

pub_type

杂志文章

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