%0 Journal Article
%T How does BAFF activate B cells in patients with autoimmune diseases?
%A Xavier Mariette
%J Arthritis Research & Therapy
%D 2012
%I BioMed Central
%R 10.1186/ar3729
%X In a study in a recent issue of Arthritis Research & Therapy, Yoshimoto and colleagues [1] demonstrate that peripheral monocytes from patients with Sj£żgren's syndrome (SS) produce significantly higher amounts of the cytokines B cell-activating factor (BAFF) (also called B-lymphocyte stimulator, or BlyS) and interleukin-6 (IL-6) in comparison with normal monocytes. Increased expression of BAFF might explain pathogenic B-cell activation in several systemic autoimmune diseases (reviewed in [2]). Interestingly, autoreactive B cells depend more on BAFF for survival than do alloreactive B cells. BAFF involvement in the pathogenesis of autoimmune diseases is well illustrated in BAFF-transgenic mice, which exhibit an autoimmune disease mimicking systemic lupus erythematosus (SLE) and primary Sj£żgren's syndrome (pSS) as well as a twofold increase in frequency of B-cell lymphoma [3]. In humans, an increased serum level of BAFF was reported in different autoimmune diseases, and findings concerning SLE and pSS were more consistent (reviewed in [2]).Recent findings showed that BAFF could be expressed and secreted by resident cell targets of autoimmunity after stimulation with different cytokines: synoviocytes in rheumatoid arthritis, astrocytes in multiple sclerosis, and epithelial cells in pSS [4]. Moreover, in the context of autoimmunity, BAFF could be secreted by T [5] and B [6] lymphocytes. However, the main sources of BAFF are myeloid cells and, especially, blood monocytes, myeloid dendritic cells, and macrophages [7].It has been suggested that monocytes from patients with autoimmune diseases were more susceptible to BAFF expression and secretion after stimulation with type 1 interferon (IFN) than those from healthy controls [8]. Yoshimoto and colleagues [1] add an important point to this discussion by emphasizing the role of monocytes in the overproduction of BAFF in autoimmunity. The authors demonstrate that peripheral pSS monocytes produce significantly higher amounts of
%U http://arthritis-research.com/content/14/1/106