Abstract:
:Silica inhalation can induce chronic lung inflammation and fibrosis. Upon silica stimulation, activated macrophages trigger the T-lymphocyte which can differentiate into many different types of Th cells, including the recently discovered Th17 cells. IL-17A, the typical Th17 cytokine, is reported in some inflammatory diseases. However, the role of IL-17A in silica-induced inflammatory response is still not clear. The regulatory mechanism of silica-induced Th17 response also needs to be investigated. So we established a mice primary cell coculture system (macrophage and lymphocyte) to investigate the role of IL-17A in silica-induced inflammatory response in vitro, by using anti-IL-17A mAb and IL-1Ra. Both anti-IL-17A mAb and IL-1Ra decreased the level of IL-17A and increased the function of Treg cells. The Th1 response was suppressed and the Th2 response was promoted by the addition of anti-IL-17A mAb or IL-1Ra. IL-1Ra treatment decreased the level of IL-6, whereas the levels of IL-23 and ROR- γ t were increased. Our study demonstrated that IL-17A reduction altered the pattern of silica-induced Th responses by boosting the function of Treg cells in vitro. Blocking the function of IL-1 signal pathway could suppress the level of IL-17A, which played the major role in modulating silica-induced Th responses in vitro.
journal_name
Mediators Inflammjournal_title
Mediators of inflammationauthors
Tang W,Liu F,Chen Y,Song L,Dai W,Li C,Weng D,Chen Jdoi
10.1155/2014/570894subject
Has Abstractpub_date
2014-01-01 00:00:00pages
570894eissn
0962-9351issn
1466-1861journal_volume
2014pub_type
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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doi:10.1155/2010/958403
更新日期:2010-01-01 00:00:00
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journal_title:Mediators of inflammation
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doi:10.1155/2018/8703172
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doi:10.1155/2014/217019
更新日期:2014-01-01 00:00:00
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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pub_type: 杂志文章,评审
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abstract::[This corrects the article DOI: 10.1155/2018/3809092.]. ...
journal_title:Mediators of inflammation
pub_type: 杂志文章,已发布勘误
doi:10.1155/2019/4524179
更新日期:2019-06-18 00:00:00