Background:The PD-1/PD-L1 axis is an important immune checkpoint for regulating immune response to various stimulants and its dysfunction may lead to the aberrant inflammation in COPD.

Objectives:To explore the role of PD-1/PD-L1 axis in the abnormal inflammation of COPD and its relationship with phenotypes of COPD.

Methods:We compare the expression of PD-L1 in DCs and its subgroups from peripheral blood mononuclear cell (PBMC) in 29 normal and 56 COPD subjects and the relationship with COPD phenotypes. We further studied the effect of PD-L1 expression in DCs and its subgroups on  functions of T cells with elastin peptide stimulation which represented as inducer to trigger abnormal inflammation in COPD progression. 

Result: In our study, the PD-L1 expression in type 1 conventioal DC (cDC1) is reduced in COPD compared with normal participants.(p=0.03, Fig. 1A) and is associated with COPD phenotype of rapid decline in lung function (p=0.02, Fig. 1B). The PD-L1 expression in cDC1 is negative correlation with CD4+ T cells (Spearman's correlation, r=-0.37, p=0.049, Fig.2A) and the lower-level of PD-L1 in cDC1 may increase proliferation of CD4+ T cells and be a trend to increase IFN-? production under elastin peptide stimulation in PBMC (p=0.04 and p=0.20, respectively, Fig.2B)

Conclusions:Lower-level PD-L1 in cDC1 is found and associated with phenotype of rapid decline of lung function in COPD. The possible mechanisms is triggerd by elastin peptide to increase CD4+ T cell proliferation and IFN-r production.