A common approach for fighting tuberculosis and leprosy: controlling endoplasmic reticulum stress in myeloid-derived suppressor cells.

Leprosy and tuberculosis are infectious diseases that are caused by bacteria, and both share primary risk factors. Mediators of these diseases are regulated by a heterogeneous immature population of myeloid cells called myeloid-derived suppressor cells (MDSCs) that exhibit immunosuppressive activity against innate and adaptive immunity. During pathological conditions, endoplasmic reticulum (ER) stress occurs in MDSCs, and high levels of ER stress affect MDSC-linked immunosuppressive activity. Investigating the role of ER stress in regulating immunosuppressive functions of MDSCs in leprosy and tuberculosis may lead to new approaches to treating these diseases. Here the authors discuss the immunoregulatory effects of ER stress in MDSCs as well as the possibility of targeting unfolded protein response elements of ER stress to diminish the immunosuppressive activity of MDSCs and reinvigorate diminished adaptive immune system responses that occur in leprosy and tuberculosis.