title: Tregs promote the differentiation of Th17 cells in silica-induced lung fibrosis in mice.
abstract: BACKGROUND
  Silicosis is an occupational lung disease caused by inhalation of silica dust and characterized by lung inflammation and fibrosis. Previous study showed that Tregs regulate the process of silicosis by modulating the maintenance of immune homeostasis in the lung. Th17 cells share reciprocal developmental pathway with Tregs and play a pivotal role in the immunopathogenesis of many lung diseases by recruiting and activating neutrophils, but the regulatory function of Tregs on Th17 response in silica induced lung fibrosis remains to be explored.
  
  
  RESULTS
  To evaluate the role of Th17 and IL-17 in the development of silicosis and their interaction with Tregs, Treg-depleted mice model was generated and exposed to silica to establish experimental model of silica-induced lung fibrosis. Here we showed that silica increased Th17 response in lung fibrosis. Tregs depletion enhanced the neutrophils accumulation and attenuated Th17 response in silica induced lung fibrosis. Both mRNA and protein results showed that Tregs exerted its modulatory function on Th17 cells and IL-17 by regulating TGF-β1 and IL-1β.
  
  
  CONCLUSIONS
  Our study suggested that Tregs could promote Th17 cells differentiation by regulating TGF-β1 and IL-1β in silica induced lung fibrosis of mice, which further the understanding of the progress of silicosis and provide a new insight in the regulatory mechanism of Th17 by Tregs in lung inflammation.
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, People's Republic of China.
authors.forename: Laiyu
authors.initials: L
authors.lastname: Song
authors.forename: Dong
authors.initials: D
authors.lastname: Weng
authors.forename: Fangwei
authors.initials: F
authors.lastname: Liu
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.forename: Cuiying
authors.initials: C
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Dong
authors.forename: Wen
authors.initials: W
authors.lastname: Tang
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D020381:Interleukin-17 / Q000378:metabolism; D053583:Interleukin-1beta / Q000096:biosynthesis; D051379:Mice; D011658:Pulmonary Fibrosis / Q000139:chemically induced*; D012829:Silicosis / Q000209:etiology* / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D058504:Th17 Cells / Q000502:physiology*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: D020381:Interleukin-17; D053583:Interleukin-1beta; D053773:Transforming Growth Factor beta1