Th17 can regulate silica-induced lung inflammation through an IL-1β-dependent mechanism.
Bottom Line: The Th17 response, which is induced by IL-1β, has been reported very important in chronic human lung inflammatory diseases.Treatment with an IL-1 type I receptor (IL-1RI) antagonist anakinra substantially decreased silica-induced lung inflammation and the Th17 response.Silica may induce IL-1β production from alveolar macrophages and promote inflammation by initiating a Th17 response via an IL-1β/IL-1RI-dependent mechanism.
Affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China; Department of Clinical Immunology, Dalian Medical University, Dalian, China.Show MeSH
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Mentions: The Th immune response is very important in the progress of lung inflammation . The massive expansion of the Th17 cell population can create an imbalance between effector T cells (such as Th1 cells) and regulatory T cells (Tregs), which determine the outcome of adaptive immune responses . We assessed the effects of IL-17 on the T cell immune response to test whether IL-17 could promote the lung inflammation of silicosis by influencing related immune responses. We examined T-bet, the key transforming growth factor of Th1 cells. IL-17 neutralization significantly increased T-bet mRNA expression in our silicosis model on days 4 and 11 (P < 0.05; Fig. 6A). CD4+IFN-γ+ Th1 cells in the spleen were increased significantly in the anti-IL-17 mAb+silica group compared with those in the control Ab + silica group on day 11 (P < 0.05; Fig. 6B). In the HLNs of anti-IL-17 mAb + silica-treated mice, CD4+IFN-γ+ Th1 cells were significantly increased in the anti-IL-17 mAb + silica group compared with those in the control Ab + silica group on days 1 and 4 (P < 0.05; Fig. 6C). These data suggest that the Th1 immune response is increased in the silicosis mouse model treated with anti-IL-17 mAb.
Affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, Shenyang, China; Department of Clinical Immunology, Dalian Medical University, Dalian, China.