Purpose of review: There is compelling evidence that the immune responses induced by crystalline silica particles are implicated in the development of silicosis. This article reviews recent observations which further delineate how innate and adaptive immunity are involved in this lung disease.
Recent findings: First, silica particles are recognized to have pathogen-associated molecular patterns by the innate immune system. The MARCO receptor expressed on the surface of macrophages appears crucial for the recognition and the uptake of silica as well as the activation of these immune cells in silicosis. Additional data support a major role of inflammation (mast cells, B lymphocytes and TNFalpha) in the development of lung fibrosis but also cancer. Silica-induced acute inflammation is accompanied by thrombosis; strongly suggesting that inhaled silica particles may also induce extrapulmonary lesions. Surprisingly, a pronounced anti-inflammatory reaction may also contribute to silica-induced lung fibrosis in mice and represent an additional etiopathogenic pathway of silicosis. Interestingly, it has been proposed that the pulmonary expression of IL-9 (a T lymphocyte-related interleukin) or Heme oxygenase-1 (an anti-inflammatory molecule) attenuated silicotic disease progression in animals.
Summary: New pathogenic routes involving innate receptors and antiinflammation as well as new antifibrotic immune mediators have been recently described in experimental silicosis, highlighting new potential therapeutic targets and strategies.