“…[11][12][13][14][15] Among those mediators implicated in the pathogenesis of silicosis, the interleukins IL-1β, IL-4, IL-5, IL-6, IL-8, and IL-10 12, [16][17][18] ; tumor necrosis factor (TNF) and its receptor sTNFR1 and sTNFR2; transforming growth factor β (TGF-β), and the chemokines CCL3 and CCL24 have been highlighted. 19,20 Other inflammatory markers such as bone morphogenetic protein (BMP2) and chemokines CCL5 and CXCL16 have been shown to mediate vascular plasticity, angiogenesis, and leukocyte recruitment in distinct tissues 21,22 and, more recently, implicated in potentiating respiratory-inflammatory processes driven by T-cells and macrophages in asthma 23,24 and viral infections. 25 One study demonstrated an association between increased expression of CCR5, which is the receptor for the CCL5 chemokine, in the development of coal workers' pneumoconiosis.…”