B10 Modulates Th Immune Response in Silica-Induced Lung Inflammation and Fibrosis in Mice
详细信息 查看官网全文
- 英文论文题名：B10 Modulates Th Immune Response in Silica-Induced Lung Inflammation and Fibrosis in Mice
- 论文作者：Fangwei Liu ; Wujing Dai ; Ying Chen ; Chao Li ; Jie Chen
- 英文论文作者：Fangwei Liu ; Wujing Dai ; Ying Chen ; Chao Li ; Jie Chen ; Division of Pneumoconiosis ; School of Public Health ; China Medical University
- 年：2016
- 作者机构：Division of Pneumoconiosis,School of Public Health,China Medical University;
- 会议召开时间：2016-11-16
- 会议录名称：第六届中国毒理学会免疫毒理专业委员会换届及学术会议资料汇编
- 语种：英文
- 分类号：R135.2
- 学会代码：ZGDV
- 会议名称：第六届中国毒理学会免疫毒理专业委员会换届及学术会议
- 会议地点：中国河南开封
- 主办单位：中国毒理学会免疫毒理专业委员会
- 学会名称：中国毒理学会
- 页数：2
- 文件大小：131k
- 原文格式：O
- 会议级别：全国
摘要
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 B10,Insufficient B10 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 B10 could exacerbate silicosis-induced lung inflammation and attenuate lung fibrosis.Multiple Th immune responses,Thl,Th2,and Thl7,were involved in B10 regulation of silica-induced lung inflammation and fibrosis.Insufficient B10 could modulate the Th immune balance toward Th 1 predominance.Insufficient B10 clearly 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 B10 could control lung inflammation and exacerbate lung fibrosis by inhibiting Thl response and modulating the Th balance.The regulatory function of B10 could be associated with Treg induction and IL-10 secretion.
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 B10,Insufficient B10 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 B10 could exacerbate silicosis-induced lung inflammation and attenuate lung fibrosis.Multiple Th immune responses,Thl,Th2,and Thl7,were involved in B10 regulation of silica-induced lung inflammation and fibrosis.Insufficient B10 could modulate the Th immune balance toward Th 1 predominance.Insufficient B10 clearly 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 B10 could control lung inflammation and exacerbate lung fibrosis by inhibiting Thl response and modulating the Th balance.The regulatory function of B10 could be associated with Treg induction and IL-10 secretion.
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 B10,Insufficient B10 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 B10 could exacerbate silicosis-induced lung inflammation and attenuate lung fibrosis.Multiple Th immune responses,Thl,Th2,and Thl7,were involved in B10 regulation of silica-induced lung inflammation and fibrosis.Insufficient B10 could modulate the Th immune balance toward Th 1 predominance.Insufficient B10 clearly 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 B10 could control lung inflammation and exacerbate lung fibrosis by inhibiting Thl response and modulating the Th balance.The regulatory function of B10 could be associated with Treg induction and IL-10 secretion.
引文