CD4 and silicosis: Many fibroblasts are activated and proliferated, releasing a large amount of collagen; silicosis progresses to diffuse interstitial fibrosis or eventually form silicotic nodules.14,15 Previous studies have demonstrated that CD4+ T cells are considered as the key participant in silicosis, and Th1/Th2 cells participate in the pathogenesis of silicosis.16,17