Chronic inflammation driven by COPD induces immunosuppressive remodeling of the TIME via activation of NF-κB and STAT3 pathways, leading to exhausted CD8+ T cells (expressing TIM-3 and LAG-3), expansion of myeloid-derived suppressor cells (MDSCs), and dysregulation of immune checkpoints including PD-L1 and CTLA-4, which may consequently attenuate ICI efficacy (13–15). Here, CD274 is linked to chronic obstructive pulmonary disease.