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Firstly, the abnormal PD-1/PD-L1 axis in COPD T cells and antigen-presenting cells suggests that immune checkpoints are involved in the chronicity of the disease: CD4 + /CD8 + T cells exhibit high expression of PD-1 with an exhausted-like phenotype, whereas PD-L1 is partially downregulated on dendritic cells, monocytes, and bronchial epithelial cells, which is associated with decreased lung function and enhanced autoimmunity (277, 278)

The multifaceted nature of AD is further complicated by a multitude of genetic and environmental risk factors, as well as diverse clinical manifestations, including the contribution of vascular pathology