Cellular and Molecular Mechanisms in Mycobacterial Infection

Dear Colleagues,

Mycobacterium tuberculosis (M.tb) caused an estimated 10 million cases of tuberculosis (TB) and 1.5 million deaths in 2018. The current TB vaccine, a live attenuated form of M. bovis named M. bovis Calmette–Guerin (BCG), provides insufficient protection. In addition, the emergence of multiple and extremely drug-resistant strains of M.tb is a growing problem. Novel vaccines and drug therapies are urgently required. The primary host cell of M.tb, the macrophage, serves as the first line of defense. Multiple pattern-recognition receptors sense mycobacterial molecular patterns, triggering intracellular signaling cascades and induction of proinflammatory cytokines, chemokines, and antimicrobial molecules. Macrophage-derived cytokines such as tumor necrosis factor, interleukin-12, IL-1β and IL-18 are critical for host defense against tuberculosis. Adaptive responses, including antigen-specific T cells, are critical in controlling the growth of M. tb by producing interferon-gamma, activating macrophages, and orchestrating granuloma formation. 

This Special Issue will cover a selection of original research articles, short communications, and current review articles in mycobacterial research, including immunity against mycobacteria, signaling transduction in TB, host–pathogen interactions, mycobacterial metabolism, drug resistance mechanisms, biomarkers of disease, and novel drugs and vaccines within the scope of molecular biology.

Dr. Natalie Eva Nieuwenhuizen

Dr. Joanna Evans
Guest Editor

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