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Quantification and role of innate lymphoid cell subsets in Chronic Obstructive Pulmonary Disease

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Abstract
Objectives: Innate lymphoid cells (ILCs) secrete cytokines, such as IFN-γ, IL-13 and IL-17, which are linked to chronic obstructive pulmonary disease (COPD). Here, we investigated the role of pulmonary ILCs in COPD pathogenesis. Methods: Lung ILC subsets in COPD and control subjects were quantified using flow cytometry and associated with clinical parameters. Tissue localisation of ILC and T-cell subsets was determined by immunohistochemistry. Mice were exposed to air or cigarette smoke (CS) for 1, 4 or 24 weeks to investigate whether pulmonary ILC numbers and activation are altered and whether they contribute to CS-induced innate inflammatory responses. Results: Quantification of lung ILC subsets demonstrated that ILC1 frequency in the total ILC population was elevated in COPD and was associated with smoking and severity of respiratory symptoms (COPD Assessment Test [CAT] score). All three ILC subsets localised near lymphoid aggregates in COPD. In the COPD mouse model, CS exposure in C57BL/6J mice increased ILC numbers at all time points, with relative increases in ILC1 in bronchoalveolar lavage (BAL) fluid. Importantly, CS exposure induced increases in neutrophils, monocytes and dendritic cells that remained elevated in Rag2/Il2rg-deficient mice that lack adaptive immune cells and ILCs. However, CS-induced CXCL1, IL-6, TNF-α and IFN-γ levels were reduced by ILC deficiency. Conclusion: The ILC1 subset is increased in COPD patients and correlates with smoking and severity of respiratory symptoms. ILCs also increase upon CS exposure in C57BL/6J mice. In the absence of adaptive immunity, ILCs contribute to CS-induced pro-inflammatory mediator release, but are redundant in CS-induced innate inflammation.
Keywords
COPD, ILC, innate inflammation, innate lymphoid cells, INFLAMMATION, PHENOTYPE, IL-17A, GAMMA, COPD

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MLA
Blomme, Evy, et al. “Quantification and Role of Innate Lymphoid Cell Subsets in Chronic Obstructive Pulmonary Disease.” CLINICAL & TRANSLATIONAL IMMUNOLOGY, vol. 10, no. 6, 2021, doi:10.1002/cti2.1287.
APA
Blomme, E., Provoost, S., De Smet, E., De Grove, K., Van Eeckhoutte, H., De Volder, J., … Maes, T. (2021). Quantification and role of innate lymphoid cell subsets in Chronic Obstructive Pulmonary Disease. CLINICAL & TRANSLATIONAL IMMUNOLOGY, 10(6). https://doi.org/10.1002/cti2.1287
Chicago author-date
Blomme, Evy, Sharen Provoost, Elise De Smet, Katrien De Grove, Hannelore Van Eeckhoutte, Joyceline De Volder, Philip M Hansbro, et al. 2021. “Quantification and Role of Innate Lymphoid Cell Subsets in Chronic Obstructive Pulmonary Disease.” CLINICAL & TRANSLATIONAL IMMUNOLOGY 10 (6). https://doi.org/10.1002/cti2.1287.
Chicago author-date (all authors)
Blomme, Evy, Sharen Provoost, Elise De Smet, Katrien De Grove, Hannelore Van Eeckhoutte, Joyceline De Volder, Philip M Hansbro, Matteo Bonato, Marina Saetta, Sara Wijnant, Fien Verhamme, Guy Joos, Ken Bracke, Guy Brusselle, and Tania Maes. 2021. “Quantification and Role of Innate Lymphoid Cell Subsets in Chronic Obstructive Pulmonary Disease.” CLINICAL & TRANSLATIONAL IMMUNOLOGY 10 (6). doi:10.1002/cti2.1287.
Vancouver
1.
Blomme E, Provoost S, De Smet E, De Grove K, Van Eeckhoutte H, De Volder J, et al. Quantification and role of innate lymphoid cell subsets in Chronic Obstructive Pulmonary Disease. CLINICAL & TRANSLATIONAL IMMUNOLOGY. 2021;10(6).
IEEE
[1]
E. Blomme et al., “Quantification and role of innate lymphoid cell subsets in Chronic Obstructive Pulmonary Disease,” CLINICAL & TRANSLATIONAL IMMUNOLOGY, vol. 10, no. 6, 2021.
@article{8714419,
  abstract     = {{Objectives: Innate lymphoid cells (ILCs) secrete cytokines, such as IFN-γ, IL-13 and IL-17, which are linked to chronic obstructive pulmonary disease (COPD). Here, we investigated the role of pulmonary ILCs in COPD pathogenesis.

Methods: Lung ILC subsets in COPD and control subjects were quantified using flow cytometry and associated with clinical parameters. Tissue localisation of ILC and T-cell subsets was determined by immunohistochemistry. Mice were exposed to air or cigarette smoke (CS) for 1, 4 or 24 weeks to investigate whether pulmonary ILC numbers and activation are altered and whether they contribute to CS-induced innate inflammatory responses.

Results: Quantification of lung ILC subsets demonstrated that ILC1 frequency in the total ILC population was elevated in COPD and was associated with smoking and severity of respiratory symptoms (COPD Assessment Test [CAT] score). All three ILC subsets localised near lymphoid aggregates in COPD. In the COPD mouse model, CS exposure in C57BL/6J mice increased ILC numbers at all time points, with relative increases in ILC1 in bronchoalveolar lavage (BAL) fluid. Importantly, CS exposure induced increases in neutrophils, monocytes and dendritic cells that remained elevated in Rag2/Il2rg-deficient mice that lack adaptive immune cells and ILCs. However, CS-induced CXCL1, IL-6, TNF-α and IFN-γ levels were reduced by ILC deficiency.

Conclusion: The ILC1 subset is increased in COPD patients and correlates with smoking and severity of respiratory symptoms. ILCs also increase upon CS exposure in C57BL/6J mice. In the absence of adaptive immunity, ILCs contribute to CS-induced pro-inflammatory mediator release, but are redundant in CS-induced innate inflammation.}},
  articleno    = {{e1287}},
  author       = {{Blomme, Evy and Provoost, Sharen and De Smet, Elise and De Grove, Katrien and Van Eeckhoutte, Hannelore and De Volder, Joyceline and Hansbro, Philip M and Bonato, Matteo and Saetta, Marina and Wijnant, Sara and Verhamme, Fien and Joos, Guy and Bracke, Ken and Brusselle, Guy and Maes, Tania}},
  issn         = {{2050-0068}},
  journal      = {{CLINICAL & TRANSLATIONAL IMMUNOLOGY}},
  keywords     = {{COPD,ILC,innate inflammation,innate lymphoid cells,INFLAMMATION,PHENOTYPE,IL-17A,GAMMA,COPD}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{16}},
  title        = {{Quantification and role of innate lymphoid cell subsets in Chronic Obstructive Pulmonary Disease}},
  url          = {{http://doi.org/10.1002/cti2.1287}},
  volume       = {{10}},
  year         = {{2021}},
}

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