When effector T cells eventually reach the infection site, bacteria can induce a multilayered immunosuppressive microenvironment, such as the induction of myeloid-derived suppressor cells (MDSCs) [62], high levels of immunosuppressive cytokines [63], and increased expression of immune checkpoint molecules such as PD-L1 and CD39 on macrophages [64], limiting the ability of T cells to control or clear Mtb at the site of lung infection, thereby inducing dysfunction in effector T cells. This evidence concerns the gene CD274 and infection.