Understanding Delayed T-Cell Priming, Lung Recruitment, and Airway Luminal T-Cell Responses in Host Defense against Pulmonary Tuberculosis

Mycobacterium tuberculosis (M.tb), the causative bacterium of pulmonary tuberculosis (TB), is a serious global health concern. Central to M.tb effective immune avoidance is its ability to modulate the early innate inflammatory response and prevent the establishment of adaptive T-cell immunity for ne...

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Main Authors: Christopher R. Shaler, Carly Horvath, Rocky Lai, Zhou Xing
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Clinical and Developmental Immunology
Online Access:http://dx.doi.org/10.1155/2012/628293
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author Christopher R. Shaler
Carly Horvath
Rocky Lai
Zhou Xing
author_facet Christopher R. Shaler
Carly Horvath
Rocky Lai
Zhou Xing
author_sort Christopher R. Shaler
collection DOAJ
description Mycobacterium tuberculosis (M.tb), the causative bacterium of pulmonary tuberculosis (TB), is a serious global health concern. Central to M.tb effective immune avoidance is its ability to modulate the early innate inflammatory response and prevent the establishment of adaptive T-cell immunity for nearly three weeks. When compared with other intracellular bacterial lung pathogens, such as Legionella pneumophila, or even closely related mycobacterial species such as M. smegmatis, this delay is astonishing. Customarily, the alveolar macrophage (AM) acts as a sentinel, detecting and alerting surrounding cells to the presence of an invader. However, in the case of M.tb, this may be impaired, thus delaying the recruitment of antigen-presenting cells (APCs) to the lung. Upon uptake by APC populations, M.tb is able to subvert and delay the processing of antigen, MHC class II loading, and the priming of effector T cell populations. This delay ultimately results in the deferred recruitment of effector T cells to not only the lung interstitium but also the airway lumen. Therefore, it is of upmost importance to dissect the mechanisms that contribute to the delayed onset of immune responses following M.tb infection. Such knowledge will help design the most effective vaccination strategies against pulmonary TB.
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spelling doaj-art-dccf3cd2ec4e4042a70288d58476fc232025-02-03T01:31:30ZengWileyClinical and Developmental Immunology1740-25221740-25302012-01-01201210.1155/2012/628293628293Understanding Delayed T-Cell Priming, Lung Recruitment, and Airway Luminal T-Cell Responses in Host Defense against Pulmonary TuberculosisChristopher R. Shaler0Carly Horvath1Rocky Lai2Zhou Xing3McMaster Immunology Research Centre; Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, L8S 4K1, CanadaMcMaster Immunology Research Centre; Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, L8S 4K1, CanadaMcMaster Immunology Research Centre; Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, L8S 4K1, CanadaMcMaster Immunology Research Centre; Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, L8S 4K1, CanadaMycobacterium tuberculosis (M.tb), the causative bacterium of pulmonary tuberculosis (TB), is a serious global health concern. Central to M.tb effective immune avoidance is its ability to modulate the early innate inflammatory response and prevent the establishment of adaptive T-cell immunity for nearly three weeks. When compared with other intracellular bacterial lung pathogens, such as Legionella pneumophila, or even closely related mycobacterial species such as M. smegmatis, this delay is astonishing. Customarily, the alveolar macrophage (AM) acts as a sentinel, detecting and alerting surrounding cells to the presence of an invader. However, in the case of M.tb, this may be impaired, thus delaying the recruitment of antigen-presenting cells (APCs) to the lung. Upon uptake by APC populations, M.tb is able to subvert and delay the processing of antigen, MHC class II loading, and the priming of effector T cell populations. This delay ultimately results in the deferred recruitment of effector T cells to not only the lung interstitium but also the airway lumen. Therefore, it is of upmost importance to dissect the mechanisms that contribute to the delayed onset of immune responses following M.tb infection. Such knowledge will help design the most effective vaccination strategies against pulmonary TB.http://dx.doi.org/10.1155/2012/628293
spellingShingle Christopher R. Shaler
Carly Horvath
Rocky Lai
Zhou Xing
Understanding Delayed T-Cell Priming, Lung Recruitment, and Airway Luminal T-Cell Responses in Host Defense against Pulmonary Tuberculosis
Clinical and Developmental Immunology
title Understanding Delayed T-Cell Priming, Lung Recruitment, and Airway Luminal T-Cell Responses in Host Defense against Pulmonary Tuberculosis
title_full Understanding Delayed T-Cell Priming, Lung Recruitment, and Airway Luminal T-Cell Responses in Host Defense against Pulmonary Tuberculosis
title_fullStr Understanding Delayed T-Cell Priming, Lung Recruitment, and Airway Luminal T-Cell Responses in Host Defense against Pulmonary Tuberculosis
title_full_unstemmed Understanding Delayed T-Cell Priming, Lung Recruitment, and Airway Luminal T-Cell Responses in Host Defense against Pulmonary Tuberculosis
title_short Understanding Delayed T-Cell Priming, Lung Recruitment, and Airway Luminal T-Cell Responses in Host Defense against Pulmonary Tuberculosis
title_sort understanding delayed t cell priming lung recruitment and airway luminal t cell responses in host defense against pulmonary tuberculosis
url http://dx.doi.org/10.1155/2012/628293
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