B cells tell scleroderma fibroblasts to produce collagen
Department of Internal Medicine, Division of Rheumatology, Patras University Hospital, 26504 Rion, Patras, Greece
Arthritis Research & Therapy 2013, 15:125 doi:10.1186/ar4392
See related research by Francois et al., http://arthritis-research.com/content/15/5/R168Published: 28 November 2013
In fibrosis fibroblasts are activated and overproduce collagen in a process with unknown drivers and equally unknown brakes that recently implicated a novel and surprising player, the B cell. B cells may be crucially involved in fibrosis in several ways: B cells may produce autoantibodies that can directly stimulate fibroblasts; B cells can produce profibrotic cytokines such as IL-6 or transforming growth factor beta; and, finally, B cells could directly stimulate fibroblasts by a contact-dependent mechanism. Recent experimental evidence suggests that B cells can enhance collagen production by fibroblasts, by a contact-dependent mechanism, and therefore are profibrotic ex vivo. These data strengthen the rationale of pursuing B-cell targeting therapies in systemic sclerosis.