AUTHOR=Chen Ying , Li Chao , Lu Yiping , Zhuang Huiying , Gu Weijia , Liu Bo , Liu Fangwei , Sun Jinkai , Yan Bo , Weng Dong , Chen Jie 

TITLE=IL-10-Producing CD1dhiCD5+ Regulatory B Cells May Play a Critical Role in Modulating Immune Homeostasis in Silicosis Patients

JOURNAL=Frontiers in Immunology

VOLUME=Volume 8 - 2017

YEAR=2017

URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2017.00110

DOI=10.3389/fimmu.2017.00110

ISSN=1664-3224

ABSTRACT=Silicosis is characterized by chronic lung inflammation and fibrosis, which are extremely harmful to human health. The pathogenesis of silicosis involves uncontrolled immune processes. Evidence supports that regulatory B cells (Bregs) produce negative regulatory cytokines, such as IL-10, which can negatively regulate immune responses in inflammation and autoimmune diseases. Our previous study found that IL-10-producing B cells (B10) were involved in the development of silica-induced lung inflammation and fibrosis of mice. However, little is known about the role of regulatory B cells in silicosis patients. In this study, we found that serum concentrations of IL-10 were significantly increased in silicosis patients by using protein array screening.We further determined that the frequency of IL-10-producing CD1dhiCD5+regulatory B cells, not IL-10-producing non-B lymphocytes, was significantly higher in silicosis patients compared to subjects under surveillance and healthy workers by flow cytometry. We also found that regulatory T cells (Tregs) and Th2 cytokines (IL-4, IL-5 and IL-13) were significantly increased in silicosis patients. Th1 cytokines (IFN-γ, IL-2 and IL-12) and inflammatory cytokines (IL-1β, IL-6 and TNF-α) were not significantly different between silicosis patients, subjects under surveillance and healthy workers. Our study indicated that IL-10-producing CD1dhiCD5+regulatory B cells might maintain Tregs and regulate Th1/Th2 polarization in silicosis patients, suggesting that IL-10-producing Bregs may play a critical role in modulating immune homeostasis in silicosis patients.