About this Research Topic
Mycobacterium tuberculosis (M. tuberculosis) is the causative agent of tuberculosis, a disease that has plagued humanity for centuries. Despite the development of vaccine called BCG (Bacillus Calmette-Guérin) over a century ago, M. Tuberculosis remains a significant infectious threat. BCG is currently the only available vaccine against tuberculosis, however other candidates are undergoing clinical trials.
BCG can trigger an immune response against M. tuberculosis., however, the bacterium itself possesses a cunning advantage: it actively suppresses the immune system. M. tuberculosis primarily infects antigen-presenting cells such as macrophages and dendritic cells. These cells can phagocytose the bacterium and present its antigens to T cells, thereby initiating an immune response. However, M. tuberculosis has evolved mechanisms to evade this process. By suppressing phagosome and lysosome fusion, autophagy is reduced, which is important for antigen processing and an effective immune response against M. tuberculosis.
Additionally, researchers have identified myeloid-derived suppressor cells (MDSCs) induced by M. Tuberculosis, and these MDSCs also contribute to immune suppression. Given the rise of drug-resistant tuberculosis, understanding M. tuberculosis’ immune evasion strategies is crucial for developing an effective vaccine or therapies which can counteract these evasive tactics.
In this Research Topic, we welcome, but by no means restrict, articles which explore the following sub-themes:
1. Immune escape by Mycobacterium tuberculosis.
2. Immunosuppression by Mycobacterium tuberculosis.
3. Host-derived immune regulation against bacterial immune escape.
4. Potential drug targets in immune regulatory pathways, or mechanisms of Mycobacterium tuberculosis.
BCG can trigger an immune response against M. tuberculosis., however, the bacterium itself possesses a cunning advantage: it actively suppresses the immune system. M. tuberculosis primarily infects antigen-presenting cells such as macrophages and dendritic cells. These cells can phagocytose the bacterium and present its antigens to T cells, thereby initiating an immune response. However, M. tuberculosis has evolved mechanisms to evade this process. By suppressing phagosome and lysosome fusion, autophagy is reduced, which is important for antigen processing and an effective immune response against M. tuberculosis.
Additionally, researchers have identified myeloid-derived suppressor cells (MDSCs) induced by M. Tuberculosis, and these MDSCs also contribute to immune suppression. Given the rise of drug-resistant tuberculosis, understanding M. tuberculosis’ immune evasion strategies is crucial for developing an effective vaccine or therapies which can counteract these evasive tactics.
In this Research Topic, we welcome, but by no means restrict, articles which explore the following sub-themes:
1. Immune escape by Mycobacterium tuberculosis.
2. Immunosuppression by Mycobacterium tuberculosis.
3. Host-derived immune regulation against bacterial immune escape.
4. Potential drug targets in immune regulatory pathways, or mechanisms of Mycobacterium tuberculosis.
Keywords: Mycobacterium tuberculosis, Tuberculosis, Immune response, T reg cells, Antigen-presenting cells, Macrophages, Dendritic cells, Infectious disease
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
