Special Issue "The Immune Escape Mechanisms of Mycobacterium tuberculosis"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: 30 November 2022 | Viewed by 734

Special Issue Editor

Dr. Vladimir V. Yeremeev
E-Mail Website
Guest Editor
Central Tuberculosis Research Institute (CTRI), Moscow, Russia
Interests: tuberculosis; biomarkers; vaccines; infection

Special Issue Information

Dear Colleagues,

The inability of the immune system to protect the host from the pathogenic effects of M. tuberculosis depends on many factors; however, two main ones can be highlighted: immune system defects at various levels and modulation of M. tuberculosis immune response that allows mycobacteria to survive, multiply, and cause a disease. As an intracellular pathogen, M. tuberculosis adapts to unfavorable external environments and not only modulates its metabolism but also affects the metabolism of the infected host cells. Understanding these metabolic changes should provide insights invaluable for the development of new approaches to tuberculosis treatment.

In this Special Issue of Cells, I invite you to contribute original research articles, reviews, or shorter perspective articles on all aspects related to the theme of “The Immune Escape Mechanisms of Mycobacterium tuberculosis”. Expert articles describing molecular, functional, cellular, biochemical, or general aspects of M. tuberculosis immune evasion are welcome. Relevant topics include but are not limited to:

  • Immune modulation
  • Dormancy
  • Phagosomal rupture
  • Cell signaling
  • Small RNAs
  • Cytokine signaling
  • Chemokine function
  • In vitro and in vivo models
  • Immunopathology of TB
  • Inflammation
  • Translational medicine

Dr. Vladimir V. Yeremeev
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (1 paper)

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Structural Variability of Lipoarabinomannan Modulates Innate Immune Responses within Infected Alveolar Epithelial Cells
Cells 2022, 11(3), 361; https://doi.org/10.3390/cells11030361 - 21 Jan 2022
Viewed by 531
Mycobacterium tuberculosis (M. tb) is an intracellular pathogen persisting in phagosomes that has the ability to escape host immune surveillance causing tuberculosis (TB). Lipoarabinomannan (LAM), as a glycolipid, is one of the complex outermost components of the mycobacterial cell envelope and [...] Read more.
Mycobacterium tuberculosis (M. tb) is an intracellular pathogen persisting in phagosomes that has the ability to escape host immune surveillance causing tuberculosis (TB). Lipoarabinomannan (LAM), as a glycolipid, is one of the complex outermost components of the mycobacterial cell envelope and plays a critical role in modulating host responses during M. tb infection. Different species within the Mycobacterium genus exhibit distinct LAM structures and elicit diverse innate immune responses. However, little is known about the mechanisms. In this study, we first constructed a LAM-truncated mutant with fewer arabinofuranose (Araf) residues named M. sm-ΔM_6387 (Mycobacterium smegmatis arabinosyltransferase EmbC gene knockout strain). It exhibited some prominent cell wall defects, including tardiness of mycobacterial migration, loss of acid-fast staining, and increased cell wall permeability. Within alveolar epithelial cells (A549) infected by M. sm-ΔM_6387, the uptake rate was lower, phagosomes with bacterial degradation appeared, and microtubule-associated protein light chain 3 (LC3) recruitment was enhanced compared to wild type Mycobacterium smegmatis (M. smegmatis). We further confirmed that the variability in the removal capability of M. sm-ΔM_6387 resulted from host cell responses rather than the changes in the mycobacterial cell envelope. Moreover, we found that M. sm-ΔM_6387 or its glycolipid extracts significantly induced expression changes in some genes related to innate immune responses, including Toll-like receptor 2 (TLR2), class A scavenger receptor (SR-A), Rubicon, LC3, tumor necrosis factor alpha (TNF-α), Bcl-2, and Bax. Therefore, our studies suggest that nonpathogenic M. smegmatis can deposit LC3 on phagosomal membranes, and the decrease in the quantity of Araf residues for LAM molecules not only impacts mycobacterial cell wall integrity but also enhances host defense responses against the intracellular pathogens and decreases phagocytosis of host cells. Full article
(This article belongs to the Special Issue The Immune Escape Mechanisms of Mycobacterium tuberculosis)
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