IL-17A Is Elevated in End-Stage Chronic Obstructive Pulmonary Disease and Contributes to Cigarette Smoke–induced Lymphoid Neogenesis

Roos, Abraham B.; Sandén, Caroline; Mori, Masataka; Bjermer, Leif; Stämpfli, Martin R.; Erjefält, Jonas

doi:10.1164/rccm.201410-1861oc

Cited by 104 publications

(98 citation statements)

References 38 publications

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“…Therefore, the CD69-deficiency-associated enhancement of IL-6 and IL-17 production may closely relate to the deterioration of emphysematous changes in CD69KO mice. IL-17 plays a crucial role in the pathogenesis of COPD mainly through recruitment of neutrophils [22]. Likewise, the degree of airflow obstruction in patients with COPD is correlated with sputum IL-17 concentrations [23].…”

Section: Effect Of Il-17-and Il-6-neutralization On Elastase-induced mentioning

confidence: 99%

Role of CD69 in the pathogenesis of elastase-induced pulmonary inflammation and emphysema

Fujita

Yoshioka

Umezawa

et al. 2016

3.2 Airway Cell Biology and Immunopathology

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Keywords: CD69 Chronic obstructive pulmonary disease IL-17 Th17 γδ T cell a b s t r a c t Cluster of differentiation 69 (CD69), known as an early activation marker of lymphocytes, has been demonstrated to regulate inflammatory events in various disease models. Although the increased number of CD69-expressed T lymphocytes in the lungs of patients with chronic obstructive pulmonary disease (COPD) has been reported, a functional role of CD69 in the pathogenesis of COPD remains unknown. To address to this question, CD69-deficient (CD69KO) mice and wild-type (WT) mice were subjected to a mouse model of porcine pancreatic elastase (PPE)-induced pulmonary inflammation and emphysema. In the two genotypes, PPE increased counts of macrophages, neutrophils and lymphocytes in bronchoalveolar lavage fluid (BALF) and induced emphysematous changes in the lung, whereas those two pathological signs were significantly enhanced in CD69KO mice compared to WT mice. Moreover, the PPE-induced levels of IL-17 and IL-6 in BALF were significantly higher in CD69KO mice than in WT mice at the acute inflammatory phase. Immunofluorescent studies showed that IL-17 and IL-6 were predominantly expressed in CD4 þ and γδ T cells and macrophages, respectively. Concomitant administration of IL-17-and IL-6-neutralizing antibodies significantly attenuated the PPE-induced emphysematous changes in the two genotypes. These findings suggest that CD69 negatively regulates the development of PPE-induced emphysema in part at least through modulating function of IL-17-producing T cells.

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Section: Effect Of Il-17-and Il-6-neutralization On Elastase-induced mentioning

confidence: 99%

Role of CD69 in the pathogenesis of elastase-induced pulmonary inflammation and emphysema

Fujita

Yoshioka

Umezawa

et al. 2016

3.2 Airway Cell Biology and Immunopathology

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“…Dres and colleagues (6) found an association between the two, whereas Laghi and colleagues (12) did not. Can these conflicting results be reconciled?…”

Section: Editorialsmentioning

confidence: 94%

“…They achieved supramaximality with certainty in only 75.8% of patients. Dres and colleagues (6) were not able to test for supramaximality because the ethics committee allowed them to deliver no more than five bilateral stimulations at a single stimulating power output (M. Dres and A. Demoule, personal communication). Thus, we do not know what proportion of the small twitches signified weakness as opposed to being the result of insufficient magnetic stimulation.…”

Section: Editorialsmentioning

confidence: 99%

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Shifting from Correlation to Causation: Challenges for the Future of Unbiased Molecular Studies in Inflammatory Lung Disease

Christenson

Steiling

2017

Am J Respir Crit Care Med

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“…A tendency toward a higher frequency of NCR - ILC3 was observed in the lungs of patients with COPD compared with the controls [62]. Additionally, IL-17A and IL-22, which are produced by NCR - ILC3s, contribute to the formation of lymphoid follicles [107, 108]. Neutrophil elastase and IL-5 levels are increased in AECOPD patients [109].…”

Section: Introductionmentioning

confidence: 99%

The origin and role of innate lymphoid cells in the lung

2016

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Innate lymphoid cells (ILCs), a newly identified member of the lymphoid population, play a critical role in the transition from innate to adaptive immunity in host defense. ILCs are important in mucosal barrier immunity, tissue homeostasis, and immune regulation throughout the body. Significant alterations in ILC responses in lung diseases have been observed and reported. Emerging evidence has shown that ILCs are importantly involved in the pathogenesis and development of a variety of lung diseases, i.e., helminth infections, allergic airway inflammation, and airway hyper-responsiveness. However, as a tissue-resident cell population, the role of ILCs in the lung remains poorly characterized. In this review, we discuss the role of ILCs in lung diseases, the mechanisms underlying the ILC-mediated regulation of immunity, and the therapeutic potential of modulating ILC responses.

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IL-17A Is Elevated in End-Stage Chronic Obstructive Pulmonary Disease and Contributes to Cigarette Smoke–induced Lymphoid Neogenesis

Abstract: IL-17A in the peripheral lung of patients with severe to very severe COPD may contribute to disease progression and development of lymphoid follicles via activation of CXCL12.

Cited by 104 publications

References 38 publications

Role of CD69 in the pathogenesis of elastase-induced pulmonary inflammation and emphysema

Role of CD69 in the pathogenesis of elastase-induced pulmonary inflammation and emphysema

Shifting from Correlation to Causation: Challenges for the Future of Unbiased Molecular Studies in Inflammatory Lung Disease

The origin and role of innate lymphoid cells in the lung

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