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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Wiley
2012-01-01
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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. |
format | Article |
id | doaj-art-dccf3cd2ec4e4042a70288d58476fc23 |
institution | Kabale University |
issn | 1740-2522 1740-2530 |
language | English |
publishDate | 2012-01-01 |
publisher | Wiley |
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series | Clinical and Developmental Immunology |
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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