title: Role of IL-10-producing regulatory B cells in modulating T-helper cell immune responses during silica-induced lung inflammation and fibrosis.
abstract: Silicosis is characterized by chronic lung inflammation and fibrosis, which are seriously harmful to human health. Previous research demonstrated that uncontrolled T-helper (Th) cell immune responses were involved in the pathogenesis of silicosis. Lymphocytes also are reported to have important roles. Existing studies on lymphocyte regulation of Th immune responses were limited to T cells, such as the regulatory T (Treg) cell, which could negatively regulate inflammation and promote the process of silicosis. However, other regulatory subsets in silicosis have not been investigated in detail, and the mechanism of immune homeostasis modulation needs further exploration. Another regulatory lymphocyte, the regulatory B cell, has recently drawn increasing attention. In this study, we comprehensively showed the role of IL-10-producing regulatory B cell (B10) in a silicosis model of mice. B10 was inducible by silica instillation. Insufficient B10 amplified inflammation and attenuated lung fibrosis by promoting the Th1 immune response. Insufficient B10 clearly inhibited Treg and decreased the level of IL-10. Our study indicated that B10 could control lung inflammation and exacerbate lung fibrosis by inhibiting Th1 response and modulating the Th balance. The regulatory function of B10 could be associated with Treg induction and IL-10 secretion.
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, P. R. China.
authors.forename: Fangwei
authors.initials: F
authors.lastname: Liu
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, P. R. China.
authors.forename: Wujing
authors.initials: W
authors.lastname: Dai
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, P. R. China.
authors.forename: Chao
authors.initials: C
authors.lastname: Li
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, P. R. China.
authors.forename: Xiaowei
authors.initials: X
authors.lastname: Lu
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, P. R. China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Department of Respiratory Medicine, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, P. R. China.
authors.forename: Dong
authors.initials: D
authors.lastname: Weng
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, P. R. China.
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
mesh_terms: D000818:Animals; D060151:B-Lymphocytes, Regulatory / Q000502:physiology*; D005260:Female; D007111:Immunity, Cellular; D016753:Interleukin-10 / Q000378:metabolism*; D008198:Lymph Nodes / Q000473:pathology; D008810:Mice, Inbred C57BL; D011658:Pulmonary Fibrosis / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism; D012822:Silicon Dioxide; D018417:Th1 Cells / Q000502:physiology*; D058504:Th17 Cells / Q000502:physiology
chemical_list: C556062:IL10 protein, mouse; D016753:Interleukin-10; D012822:Silicon Dioxide