How does BAFF activate B cells in patients with autoimmune diseases?
Service de Rhumatologie, Hôpital Bicêtre, Assistance Publique-Hôpitaux de Paris (AP-HP), Université Paris-Sud, Institut Pour la Santé et la Recherche Médicale (INSERM) U 1012, 78 rue du Général Leclerc, 94275 Le Kremlin Bicêtre, France
Arthritis Research & Therapy 2012, 14:106 doi:10.1186/ar3729
See related research by Yoshimoto et al., http://arthritis-research.com/content/13/5/R170Published: 24 February 2012
In a study in a recent issue of Arthritis Research & Therapy, Yoshimoto and colleagues demonstrate that peripheral monocytes from patients with Sjögren's syndrome (SS) produce significantly higher amounts of B cell-activating factor (BAFF) and interleukin-6 (IL-6) in comparison with normal monocytes. This difference exists at baseline and is amplified after stimulation with interferon-gamma. Increased IL-6 secretion is partially suppressed by an anti-BAFF antibody, suggesting that signal transduction pathways mediated by BAFF are implicated in the regulation of IL-6 production by monocytes. The origin and pathways involved in this higher susceptibility to BAFF-driven IL-6 induction by monocytes of patients with SS are still unknown.