Introduction: 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.Material and Method:To evaluate the role of B 10, Insufficient B 10 in mice model was generated using anti-CD22 mAb and exposed to silica to establish experimental model of silica-induced lung fibrosis.Flow cytometry was used to check the phenotype of immune cells.Pathological examination was performed to confirm the progress of silica-induce lung fibrosis.CBA and realtime-PCR were used to test the changes of related inflammatory cytokines.Results: In this study, we comprehensively showed the role of IL-10-producing regulatory B cell (B10) in a silicosis model of mice.Insufficient B 10 could exacerbate silicosis-induced lung inflammation and attenuate lung fibrosis.Multiple Th immune responses, Th1, Th2, and Th1 7, were involved in B 10 regulation of silica-induced lung inflammation and fibrosis.Insufficient B 10 could modulate the Th immune balance toward Th1 predominance.Insufficient B10clearly inhibited Treg and decreased the level of IL-10.Depletion of Treg only slightly affect the number of B10 at early inflammation stage.Conclusion: Our study indicated that B 10 could control lung inflammation and exacerbate lung fibrosis by inhibiting Th 1 response and modulating the Th balance.The regulatory function of B10 could be associated with Treg induction and IL-10 secretion.