CXCR5/CXCL13 pathway, a key driver for migration of regulatory B10 cells, is defective in patients with rheumatoid arthritis.

Claire RempenaultJulie MielleKristina SchreiberPierre CorbeauLaurence MaciaBernard CombeJacques MorelClaire Immediato DaienRachel Audo

Published in: Rheumatology (Oxford, England) (2021)

Our results identify that the CXCR5/CXCL13 axis is essential for B10+ cell biology but is defective in RA. Restoring the preferential migration of B10+ within the affected joints to better control inflammation may be part of therapeutic approach for RA.

Keyphrases

rheumatoid arthritis
disease activity
oxidative stress
cell migration
ankylosing spondylitis
interstitial lung disease
systemic lupus erythematosus
systemic sclerosis