CXCL10 recruits activated T cells, NK cells, and to a lesser extent, macrophages and dendritic cells to sites of infection [50], and enhances Th1 polarization by acting on CXCR3 + naïve T cells—establishing a positive feedback loop between IFN-γ-producing Th1 cells and CXCL10-producing resident cells [51]. The gene discussed is CXCL10; the disease is infection.