In contrast, during acute and chronic inflammation, M1 inflammatory subsets have been reported to drastically recruit immune cells to the site of infection, skewing the cytokine balance and stimulating an inflammatory response by releasing cytokines or chemokines including interferon γ (IFN-γ), IL-6, TNF-α, IL-1β, CCL5, and C-X-C motif chemokine ligand 10 (CXCL10) (Gerdprasert et al., 2002; Mantovani et al., 2004; Biswas and Mantovani, 2010; Geissmann et al., 2010; Locati et al., 2013; Murray et al., 2014; Li et al., 2019). This evidence concerns the gene CXCL10 and infection.