Breaching the Defenses? Mucosal-associated Invariant T Cells, Smoking, and Chronic Obstructive Pulmonary Disease
Breaching the Defenses? Mucosal-associated Invariant T Cells, Smoking, and Chronic Obstructive Pulmonary Disease
There can be little doubt that cigarette smoking is one of the primary causes of chronic obstructive pulmonary disease (COPD), however the precise mechanisms by which cigarette smoke (CS) exposure leads to COPD are yet to be elucidated. Ample evidence suggests CS causes substantial changes to the epithelial barrier (1) as well as immune cells (2) that persist in COPD. Furthermore, these changes are also associated with microbial dysbiosis in the airways of COPD patients (3), an important driver of COPD exacerbations and mortality (4, 5). In this issue of the Journal, Huber et al further investigate the impact of both smoking and COPD on the interaction between epithelial cells and mucosal-associated invariant T (MAIT) cells (6). MAIT cells are innate-like T cells, which play a role in controlling bacterial infection by recognizing non-peptide antigens derived from the bacterial vitamin B2 pathway presented by the MHC-related protein (MR)-1 (7).
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Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee
1 January 2023
Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee
Staples, Karl J.
(2023)
Breaching the Defenses? Mucosal-associated Invariant T Cells, Smoking, and Chronic Obstructive Pulmonary Disease.
American Journal of Respiratory Cell and Molecular Biology, 68 (1), .
(doi:10.1165/rcmb.2022-0393ED).
Abstract
There can be little doubt that cigarette smoking is one of the primary causes of chronic obstructive pulmonary disease (COPD), however the precise mechanisms by which cigarette smoke (CS) exposure leads to COPD are yet to be elucidated. Ample evidence suggests CS causes substantial changes to the epithelial barrier (1) as well as immune cells (2) that persist in COPD. Furthermore, these changes are also associated with microbial dysbiosis in the airways of COPD patients (3), an important driver of COPD exacerbations and mortality (4, 5). In this issue of the Journal, Huber et al further investigate the impact of both smoking and COPD on the interaction between epithelial cells and mucosal-associated invariant T (MAIT) cells (6). MAIT cells are innate-like T cells, which play a role in controlling bacterial infection by recognizing non-peptide antigens derived from the bacterial vitamin B2 pathway presented by the MHC-related protein (MR)-1 (7).
Text
Staples editorial 2022-09-27
- Accepted Manuscript
More information
Accepted/In Press date: 17 October 2022
e-pub ahead of print date: 18 October 2022
Published date: 1 January 2023
Identifiers
Local EPrints ID: 471592
URI: http://eprints.soton.ac.uk/id/eprint/471592
ISSN: 1044-1549
PURE UUID: 42b75654-140d-40f4-a39e-0e4162275e97
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Date deposited: 14 Nov 2022 17:47
Last modified: 17 Mar 2024 07:34
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