Impact of Treg on other T cell subsets in progression of fibrosis in experimental lung fibrosis.

Idiopathic pulmonary fibrosis is an irreversible, progressive and lethal lung disease. Regulatory T cells (Tregs) and Th17 cells both are involved in lung fibrosis. But there are only few reports regarding the effect of Treg on other T cell subsets in experimental lung fibrosis. The aim of this study was to investigate the impact of Treg on Th17, CD4+CD28-T, CD4+CD28+T and CD8 + T cell subsets that could drive lung fibrosis. To reach the goal of our study, first we depleted Tregs by anti-CD25 mAb injection in experimental C57BL/6 mice model. It has been demonstrated in our study that depletion of Treg ameliorates bleomycin-induced lung fibrosis by immune modulating Th17 and other important T cell subsets response in lung. Our flow cytometry data revealed that the percentages of Th17, CD4+CD28-T, CD4+CD28+T and CD8 + T cell subsets were decreased in experimental lung fibrosis after Treg depletion. We also observed significant downregulation of IL-17 A in Treg-depleted mice after bleomycin delivery. In addition, the study also suggested that Treg depletion led to considerable upregulation of IFN-γ after bleomycin administration. Therefore, Th17 cells, CD8 + T cells, CD4+CD28- and CD4+CD28+ T cell subsets all are controlled by regulatory T cell, help in progression of fibrosis in experimental lung fibrosis.