The expression of Foxp3 and ROR gamma t in lung tissues from normal smokers and chronic obstructive pulmonary disease patients

Chu, Shaoli; Zhong, Xiaoning; Zhang, Jianquan; Lao, Qifang; Zhou, He; Bai, Jing

doi:10.1016/j.intimp.2011.06.010

Cited by 44 publications

(47 citation statements)

References 36 publications

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“…Finally, there is growing evidence to suggest that patients with COPD have higher proportions of T H 17 cells among their peripheral blood mononuclear cells (PBMC) and high levels of IL-17A and IL-17F on bronchial biopsies 125, 126 . High levels of RORγT mRNA have also been reported in the lungs of patients with COPD 127 . However, a phase II trial of anti-IL-17A Ab (CNTO 6785) did not show any significant efficacy in the treatment of patients with symptomatic moderate-to-severe COPD 128 .…”

Section: Il-17 In the Lungsmentioning

confidence: 95%

Mucocutaneous IL-17 immunity in mice and humans: host defense vs. excessive inflammation

2018

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Interleukin (IL)-17A is a pro-inflammatory cytokine in mice and humans. It is recognized as a key factor for the protection of mice against various pathogens, but it also underlies pathogenic inflammatory responses in numerous mouse models. The inborn errors of IL-17A- and IL-17F-mediated immunity identified in humans in the last decade have revealed that IL-17A and IL-17F are key players in mucocutaneous immunity to Candida albicans, and, to a lesser extent, Staphylococcus aureus. By contrast, there is currently no genetic evidence for a causal link between excess of IL-17 and autoimmunity, autoinflammation, or allergy in humans. We discuss here the physiological and pathological roles of mouse and human IL-17A and IL-17F in host defense and excessive inflammation. We highlight recent advances in our understanding of the consequences deficient or excessive IL-17 immunity at various mucocutaneous sites, including the oral cavity, skin, intestine, lungs, and vagina.

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Section: Il-17 In the Lungsmentioning

confidence: 95%

Mucocutaneous IL-17 immunity in mice and humans: host defense vs. excessive inflammation

2018

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“…Chronic obstructive pulmonary disease (COPD) has been proposed as a target for T H 17-based therapy. Cigarette smoke, the Nature Reviews | Drug Discovery In addition to the effector cytokines IL-17A or IL-17F, expression of RORC2 (the transcription factor that controls the differentiation of T H 17 cells) is increased in the lungs of patients with COPD 139,136 . Studies from transgenic mice provide further evidence that IL-17 is involved in the pathogenesis of lung disease.…”

Section: Vasculitis and Atherosclerosismentioning

confidence: 99%

Targeting IL-17 and TH17 cells in chronic inflammation

Miossec

Kolls

2012

Nat Rev Drug Discov

1,117

894

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The key role of interleukin-17 (IL-17) and T helper 17 (T(H)17) cells in tissue inflammation, autoimmunity and host defence led to the experimental targeting of these molecules in mouse models of diseases as well as in clinical settings. Moreover, the demonstration that IL-17 and T(H)17 cells contribute to local and systemic aspects of disease pathogenesis, as well as the finding that the IL-17-T(H)17 cell pathway is regulated by IL-23, prompted the identification of inhibitors. These inhibitors include biotechnology products that target IL-23 as well as the leading member of the IL-17 family, IL-17A, and one of its receptors, IL-17 receptor A. Several clinical trials of these inhibitors are underway, and positive results have been obtained in psoriasis, rheumatoid arthritis and ankylosing spondylitis. This Review focuses on the current knowledge of the IL-17-T(H)17 cell pathway to better understand the positive as well as potential negative consequences of targeting them.

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“…IL-17 is associated with increased mucus production and airway inflammation with production of the neutrophil chemoattractant CXCL-8 and neutrophilia. 6,7 In a metastatic melanoma model, blocking of CTLA-4 increased numbers of circulating Th17 cells and the production of IL-17. 10 Hence, poor induction of CTLA-4 may promote Th17-mediated inflammation in patients with COPD or chronic bronchitis.…”

Section: Cd4mentioning

confidence: 99%

“…4,5 Accumulation of interleukin (IL)-17-producing T cells in the bronchial submucosa and alveolar wall of COPD patients may promote the neutrophilic airway inflammation characteristic of COPD. 6,7 Despite evidence of the role of T cells, mechanisms underlying T-cell dysregulation in COPD are unclear. CTLA-4 is an important negative regulator of T-cell activity.…”

mentioning

confidence: 99%