These results suggested that Th1 cells and/or Th1 cytokines benefited from the severer neutrophilic inflammation in experimental model of silica-induced lung fibrosis in the absence of Tregs; since the differentiation of Th17 cells could be inhibited by the Th1 cytokine [12], enhancement of Th1 cytokines might inhibit Th17 differentiation and IL-17 secretion. Here, IL17A is linked to pulmonary fibrosis.