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Review
. 2022 Jul 6;11(14):2132.
doi: 10.3390/cells11142132.

IL-17 Cytokines and Chronic Lung Diseases

Felix Ritzmann  1   2 , Lars Peter Lunding  3   4 , Robert Bals  1   2 , Michael Wegmann  3   4 , Christoph Beisswenger  1
Affiliations
Review

IL-17 Cytokines and Chronic Lung Diseases

Felix Ritzmann et al. Cells. .

Abstract

IL-17 cytokines are expressed by numerous cells (e.g., gamma delta (γδ) T, innate lymphoid (ILC), Th17, epithelial cells). They contribute to the elimination of bacteria through the induction of cytokines and chemokines which mediate the recruitment of inflammatory cells to the site of infection. However, IL-17-driven inflammation also likely promotes the progression of chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), lung cancer, cystic fibrosis, and asthma. In this review, we highlight the role of IL-17 cytokines in chronic lung diseases.

Keywords: IL-17; infection; inflammation; lung damage; lung diseases.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Figure 1
Figure 1
IL-17 cytokines mediate the recruitment of immune cells. (A) IL-17 cytokine and receptor family. To which receptors (?) IL-17B and IL-17D bind remains to be elucidated. (B) Infection results in the release of IL-17A from immune cells (γδ T, innate lymphoid (ILC), Th17 cells). IL-17A activates lung epithelial cells, resulting in enhanced chemokine-mediated recruitment of immune cells (e.g., neutrophils) and enhanced expression (formula image) of mucins and antimicrobial peptides (AMP). (C) Bacteria and viruses induce the expression of IL-17C in lung epithelial cells. IL-17C enhances the expression of cytokines and chemokines in an autocrine manner, resulting in increased pulmonary inflammation.
Figure 2
Figure 2
IL-17 cytokines promote the progression of chronic lung diseases. Acute and chronic infections or disease-associated microbiota drive the expression of IL-17 in immune and epithelial cells. IL-17-mediated expression of cytokines and recruitment of inflammatory cells, mainly neutrophils, result in airway remodeling (e.g., goblet cell hyperplasia) and lung damage in COPD, CF, and asthma (A) as well as in tumor proliferation and resistance to immunotherapy in lung cancer (B).
See this image and copyright information in PMC

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