Considering IL-22, less than 10 % of IL-22+ cells were T cells and more than 80 % of IL-22+ cells were also CD31+ endothelial cells, suggesting that the contribution of T cells in producing the IL-17-related cytokines and their possible related neutrophilic effects is relatively modest and that surprisingly, endothelial cells contribute importantly to the total upregulation of these cytokines in the bronchial mucosa of COPD patients [39]. This evidence concerns the gene IL17A and chronic obstructive pulmonary disease.