Furthermore, miR-199a-3p can mediate immune tolerance by regulating dendritic cells, leading to increased secretion of interleukin 10 as well as to the inhibition of the phosphatidylinositol 3-kinase/protein kinase B/nuclear factor kappa B pathway, and miR-16 was significantly upregulated in the serum of patients with TB compared with healthy controls [46,47]. Here, IL10 is linked to tuberculosis.