PM induces the aggregation of CD8+ T cells in the subepithelial layer of the airway and the alveolar septum of rats with COPD, to releases granzyme B and perforin, leading to an increase in cytotoxic T lymphocyte (CTL) response and resulting in lung tissue damage (47), It may be related to the fact that PM stimulates BM-DCs to highly express CD83/CCR7, thereby promoting the proliferation of CD8+ T cells (48). This evidence concerns the gene CD8A and chronic obstructive pulmonary disease.