The role of CD8 + T lymphocytes in chronic obstructive pulmonary disease: a systematic review

Objective and design This systematic review aims to establish the role of CD8 + T lymphocytes in COPD. Methods Forty-eight papers published in the last 15 years were identified for inclusion. Results CD8 + T-cells are increased in the lungs of patients with COPD (17 studies, 16 positive) whereas in...

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Bibliographic Details
Published in:Inflammation research 2021-01, Vol.70 (1), p.11-18
Main Authors: Williams, Maya, Todd, Ian, Fairclough, Lucy C.
Format: Article
Language:English
Subjects:
Allergology
Alveoli
Biomedical and Life Sciences
Biomedicine
CD8 antigen
Cell activation
Chronic obstructive pulmonary disease
Cytotoxicity
Dermatology
Immunology
Lung diseases
Lungs
Lymphocytes
Lymphocytes T
Neurology
Obstructive lung disease
Pathogenesis
Pharmacology/Toxicology
Phenotypes
Review
Rheumatology
Systematic review
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Summary:Objective and design This systematic review aims to establish the role of CD8 + T lymphocytes in COPD. Methods Forty-eight papers published in the last 15 years were identified for inclusion. Results CD8 + T-cells are increased in the lungs of patients with COPD (17 studies, 16 positive) whereas in the circulation, findings were inconclusive. Activation of CD8 + T-cells was enhanced in lungs (four studies, three positive) but cell phenotype was unclear. There was substantial evidence of a higher proportion of type 1 CD8 + (Tc1) cells in COPD (11 studies, 9 positive), though the population of type 2 (Tc2) cells was also increased (5 studies, 4 positive). CD8 + T-cells in COPD exhibited greater expression of cytotoxic proteins (five studies, five positive). Studies assessed a variety of questions so evidence was insufficient to draw firm conclusions. The role of CD8 + T-cells at acute exacerbation of COPD and also their contribution to alveolar destruction can only be hypothesised at this stage. Conclusions Not only is the number of CD8 + T-cells increased in COPD, these cells have increased capacity to exert effector functions and are likely to contribute to disease pathogenesis. Several mechanisms highlighted show promise for future investigation to consolidate current knowledge.
ISSN:1023-3830
1420-908X
DOI:10.1007/s00011-020-01408-z