Further, in NE-COPD, where PPARγ macrophages were relatively increased, pairwise comparisons of ligand-receptor activities predicted increased interactions between PPARγ macrophages with NR3C1+ CD4 T cells through integrins, cell adhesion molecules and chemokine/cytokine receptors such as ITGB2, ALCAM, and CXCR4 (Supplementary Fig. 7a–c). This evidence concerns the gene CD4 and chronic obstructive pulmonary disease.