Abstract
The encounter between Mycobacterium tuberculosis (Mtb) and the host leads to a complex and multifaceted immune response possibly resulting in latent infection, tubercular disease or to the complete clearance of the pathogen. Macrophages and CD4+ T lymphocytes, together with granuloma formation, are traditionally considered the pillars of immune defense against Mtb and their role stands out clearly. However, there is no component of the immune system that does not take part in the response to this pathogen. On the other side, Mtb displays a complex artillery of immune-escaping mechanisms capable of responding in an equally varied manner. In addition, the role of each cellular line has become discussed and uncertain further than ever before. Each defense mechanism is based on a subtle balance that, if altered, can lean to one side to favor Mtb proliferation, resulting in disease progression and on the other to the host tissue damage by the immune system itself. Through a brief and complete overview of the role of each cell type involved in the Mtb response, we aimed to highlight the main literature reviews and the most relevant studies in order to facilitate the approach to such a complex and changeable topic. In conclusion, this narrative mini-review summarizes the various immunologic mechanisms which modulate the individual ability to fight Mtb infection taking in account the major host and pathogen determinants in the susceptibility to tuberculosis.
Highlights
Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb) infection, was among the top 10 causes of death worldwide in 2017 with about 1.5 million registered deceases (1)
The success of Mtb over thousands of years against man arises from its extraordinary ability to subvert the mechanisms that should eliminate it in the M from the infection onset
At the onset of the infection, Mtb manages to perforate the phagosome in the M through the ESX system and, to block its maturation via nucleoside diphosphate kinase (Npk), which inhibits lysosomal traffic and NADPH-oxidase activity (31)
Summary
Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb) infection, was among the top 10 causes of death worldwide in 2017 with about 1.5 million registered deceases (1). Mtb was responsible for approximately 10.0 million incident cases of TB disease with 10% of these occurring among children (1). Mtb encounters a first line of defense consisting of airway epithelial cells (AECs) and “professional” phagocytes (neutrophils, monocytes and dendritic cells) (3, 4). If this first line succeeds in eliminating the Mtb rapidly, the infection aborts (5). Phagocytes are infected and the Mtb reproduces inside the cells, initially causing few, if any, clinical manifestations (5). The establishment of the infection, the development of active TB (ATB) rather than latent TB infection (LTBI) and the eventual evolution of LTBI to ATB depends on the complex relation between bacterial and host factors
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