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Highly Accessed Editorial

B cells tell scleroderma fibroblasts to produce collagen

Dimitrios Daoussis* and Stamatis-Nick C Liossis

Author Affiliations

Department of Internal Medicine, Division of Rheumatology, Patras University Hospital, 26504 Rion, Patras, Greece

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Arthritis Research & Therapy 2013, 15:125  doi:10.1186/ar4392


See related research by Francois et al., http://arthritis-research.com/content/15/5/R168

Published: 28 November 2013

Abstract

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.