The Ambiguous Role of Macrophages in Pulmonary Tuberculosis

Abstract

Tuberculosis persists among the top 10 causes of death globally; causing 1.7 million deaths and 10 million new infections in 2018. Approximately 1/3 of the global population is infected with Mycobacterium tuberculosis; 10% of which are expected to develop active TB at some point in their life. The high burden of tuberculosis in the world is owed to lack of adherence to treatment, diminishment in treatment options and post-infection bacterial metabolic dormancy called latent TB (LTB), along with logistic, financial and political obstacles impeding successful TB control programs globally. Infections with M. tuberculosis leave no component of the immune system unengaged, hallmarked with granulomatous pathology as a function of the adaptive immune system. The hallmark of infection is a granulomatous pathological course, with the purpose of containing the difficult-to-kill bacilli, although the nature of the granuloma remains moot. The cells responsible for granuloma formation are professional alveolar macrophages, which seem to have both a beneficial and detrimental role in TB immunopathology. Herein, we discuss relevant immunological intricacies of macrophages in TB, ranging from immunogenetics, receptor-mediated uptake, macrophage-mediated immunopathology and the infamous tuberculosis granuloma.