Abstract
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.
Highlights
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
The authors demonstrate that peripheral primary Sjögren’s syndrome (pSS) monocytes produce significantly higher amounts of BAFF and IL-6 in comparison with normal monocytes
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
Summary
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. In a study in a recent issue of Arthritis Research & Therapy, Yoshimoto and colleagues [1] demonstrate that peripheral monocytes from patients with Sjögren’s syndrome (SS) produce significantly higher amounts of the cytokines B cell-activating factor (BAFF) ( 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]).
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