Objective To understand the expression of OX62 and CD83 in the lungs of rats with COPD, and to investigate the effect of the CCL20 monoclonal antibody on it. Methods A total of 30 rats were randomly divided into three groups: normal, model, and CCL20 antibody treated. COPD was induced by cigarette smoke exposure 28 days and LPS solution injection twice. The rats were injected with CCL20 antibody in the last group on the first day. The rats were sacrificed on the 29th day. We investigated the pathomorphology of their lungs by HE staining and evaluated the DC distribution in their lungs by immunohistochemistry. Results The HE staining results of the COPD models are consistent with the typical pathological features of COPD patients, the lung pathology in CCL20 group was significantly attenuated than that in the COPD group. Compared with healthy control group, the OX62+DCs in the COPD model group was significantly increased (P < 0.05), and the CCL20 group was lower than that in the COPD group (P < 0.05). The CD83+ DCs of COPD group was lower than that in healthy control group (P < 0.05), and the difference was not statistically significant between COPD and CCL20 treated group (P > 0.05). Conclusion The pathogenesis of COPD may be related to the increase of OX62+DC and the decrease of CD83+DC, and this effect could be partly inhibited by CCL20 antibody.