Abstract
Idiopathic Pulmonary fibrosis (IPF) is a deadly progressive lung disease with very few treatment options till now. Chronic inflammation and progressive fibrosis of the pulmonary interstitial tissues are the main features for pulmonary fibrosis (PF). Bleomycin (BLM)-induced pulmonary fibrosis (BIPF) is a commonly used mice model in IPF research. TGF-β1 (transforming growth factor-beta 1) has been shown to play a key role in pulmonary fibrosis. The coexistence of chronic inflammation sustained by mature dendritic cells (DCs) with fibrosis suggests that inflammatory phenomenon has key importance in the pathogenesis of pulmonary fibrosis. Here, we investigated the effect of TGF-β upon DCs phenotypic maturation, migration and accumulation in lung tissue in PF. Accumulation and phenotypic maturation of lung CD11c+DCs is differentially modulated by TGF-β in two different phases of the disease. TGF-β inhibits up-regulation of CD86 and CD80 markers on lung CD11c+ DCs in BIPF. Down-regulation of both the lung DC subsets CD11c+CD103+CD11b- and CD11c+CD11b+CD103- by TGF-β is observed in our study. Expression of plasmacytoid DCs is not so modulated in presence or absence of TGF-β. On the other side, enhanced expression of migratory receptor (CCR7) on lung CD11c+ is media ted by TGF-β. In summary, these data demonstrates differential modulation of CD11c+ lung DCs by TGF-β in PF.
- Copyright ©the authors 2016
