Among them, CD163 was significantly upregulated in FABP4+ MΦ, FCN1+ MΦ, and SELENOP+ MΦ subsets in the HIV-1–TB group, suggesting that these macrophage subsets tend to exhibit M2-like anti-inflammatory phenotype in people with HIV-1–TB coinfection (Figure 4A). Here, SELENOP is linked to tuberculosis.