Mycobacterium tuberculosis (M. tb) is an extremely successful pathogen that has coevolved with humans for thousands of years. Infection outcome depends upon the bacilli’s interaction with the host immune system. Both innate and adaptive immunity modify the course of M. tb infection, which may result in elimination of the bacilli, establishment of latent infection or development of active disease.
Virulent strains of M. tb possess various strategies to manipulate host immunity to their own advantage. This may include interfering with the initial recognition as well as harnessing various mechanisms that help the bacilli to survive within target cells. The adaptation to the host is orchestrated by mycobacterial factors that counteract antibacterial means of the host including maturation of phagocytic cells and various effector functions. Such early immune modulation has major downstream consequences resulting in altered protective immune responses or pathological inflammation and tissue damage.
Immune modulations employed by M. tb interfere with multiple pathways of host innate and adaptive immunity in favor of persistent infection and disease progression. To mention a few, the expression or function of human leukocyte antigens (HLA), toll like receptors (TLR), vitamin D receptors (VDR), cytokines with their receptors are among the immune components that are recognized to be altered. M. tb can also target and modify the molecular regulatory machinery of host immunity as well as its own gene expression to bias or attenuate the immune response of the host.
Although the immune evasion mechanisms identified so far are already numerous, they most likely represent only the tip of the iceberg by which the pathogen achieves its extraordinary ability to persist within the human host. An in-depth understanding of possible mechanisms by which the bacilli establishes to modulate the immune response of the host remains critical in the quest for more effective vaccines and therapeutic targets. This will also significantly impact the effort to reduce TB incidence in particular MDR and XDR-TB and reach the global End TB targets. In this Research Topic, we aim to present emerging strategies and developments employed by M. tb in modifying the host immune machinery for its own advantage. We welcome the submission of Reviews (Mini Reviews, Reviews, Opinions) as well as novel Original Research articles focusing on, but not strictly limited to, the following topics:
• Novel strategies employed by M. tb in modulating host innate and adaptive immune cells activation and effector function
• Potential mechanisms for how M. tb influences hematopoietic stem cells and their implications on host trained immunity as well as vaccine responses
• Identification of possible targets within immune pathways that may be harnessed to strengthen host cell functions and counterattack the immune evasion strategies employed by M. tb
• Identification of mechanisms for how M. tb may hijack the host immune response and the possible pathological implications for the host
• Novel assays/tools that could help in characterizing immune and microbial responses to establish a comprehensive overview of the immune evasion networks and beyond
• Mechanisms for the potential beneficial effects of M. tb on the immune response to other pathogens and disease conditions with regard to trained immunity.
Mycobacterium tuberculosis (M. tb) is an extremely successful pathogen that has coevolved with humans for thousands of years. Infection outcome depends upon the bacilli’s interaction with the host immune system. Both innate and adaptive immunity modify the course of M. tb infection, which may result in elimination of the bacilli, establishment of latent infection or development of active disease.
Virulent strains of M. tb possess various strategies to manipulate host immunity to their own advantage. This may include interfering with the initial recognition as well as harnessing various mechanisms that help the bacilli to survive within target cells. The adaptation to the host is orchestrated by mycobacterial factors that counteract antibacterial means of the host including maturation of phagocytic cells and various effector functions. Such early immune modulation has major downstream consequences resulting in altered protective immune responses or pathological inflammation and tissue damage.
Immune modulations employed by M. tb interfere with multiple pathways of host innate and adaptive immunity in favor of persistent infection and disease progression. To mention a few, the expression or function of human leukocyte antigens (HLA), toll like receptors (TLR), vitamin D receptors (VDR), cytokines with their receptors are among the immune components that are recognized to be altered. M. tb can also target and modify the molecular regulatory machinery of host immunity as well as its own gene expression to bias or attenuate the immune response of the host.
Although the immune evasion mechanisms identified so far are already numerous, they most likely represent only the tip of the iceberg by which the pathogen achieves its extraordinary ability to persist within the human host. An in-depth understanding of possible mechanisms by which the bacilli establishes to modulate the immune response of the host remains critical in the quest for more effective vaccines and therapeutic targets. This will also significantly impact the effort to reduce TB incidence in particular MDR and XDR-TB and reach the global End TB targets. In this Research Topic, we aim to present emerging strategies and developments employed by M. tb in modifying the host immune machinery for its own advantage. We welcome the submission of Reviews (Mini Reviews, Reviews, Opinions) as well as novel Original Research articles focusing on, but not strictly limited to, the following topics:
• Novel strategies employed by M. tb in modulating host innate and adaptive immune cells activation and effector function
• Potential mechanisms for how M. tb influences hematopoietic stem cells and their implications on host trained immunity as well as vaccine responses
• Identification of possible targets within immune pathways that may be harnessed to strengthen host cell functions and counterattack the immune evasion strategies employed by M. tb
• Identification of mechanisms for how M. tb may hijack the host immune response and the possible pathological implications for the host
• Novel assays/tools that could help in characterizing immune and microbial responses to establish a comprehensive overview of the immune evasion networks and beyond
• Mechanisms for the potential beneficial effects of M. tb on the immune response to other pathogens and disease conditions with regard to trained immunity.
