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Mycobacterium tuberculosis and myeloid-derived suppressor cells: Insights into caveolin rich lipid rafts. | LitMetric

Mycobacterium tuberculosis and myeloid-derived suppressor cells: Insights into caveolin rich lipid rafts.

EBioMedicine

DST-NRF Centre of Excellence for Biomedical Tuberculosis Research, South African Medical Research Council for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medical and Health Sciences, Stellenbosch University, Cape Town, South Africa. Electronic address:

Published: March 2020

AI Article Synopsis

  • Mycobacterium tuberculosis (M.tb) is an extraordinarily successful pathogen that avoids the human immune system while altering metabolism for its growth.
  • Ineffective immune responses lead to the persistence of the bacteria and the progression of tuberculosis (TB) disease.
  • The review highlights the need for research on how myeloid-derived suppressor cells (MDSC) internalize M.tb and manipulate host lipids to enhance the bacteria's survival, which could lead to improved anti-TB treatments.

Article Abstract

Mycobacterium tuberculosis (M.tb) is likely the most successful human pathogen, capable of evading protective host immune responses and driving metabolic changes to support its own survival and growth. Ineffective innate and adaptive immune responses inhibit effective clearance of the bacteria from the human host, resulting in the progression to active TB disease. Many regulatory mechanisms exist to prevent immunopathology, however, chronic infections result in the overproduction of regulatory myeloid cells, like myeloid-derived suppressor cells (MDSC), which actively suppress protective host T lymphocyte responses among other immunosuppressive mechanisms. The mechanisms of M.tb internalization by MDSC and the involvement of host-derived lipid acquisition, have not been fully elucidated. Targeted research aimed at investigating MDSC impact on phagocytic control of M.tb, would be advantageous to our collective anti-TB arsenal. In this review we propose a mechanism by which M.tb may be internalized by MDSC and survive via the manipulation of host-derived lipid sources.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7047144PMC
http://dx.doi.org/10.1016/j.ebiom.2020.102670DOI Listing

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