IL-33/ST2 axis controls Th2/IL-31 and Th17 immune response in allergic airway diseases

Vocca, Lavinia; Sano, Caterina Di; Uasuf, Carina Gabriela; Sala, Angelo; Riccobono, Loredana; Gangemi, Sebastiano; Albano, Giusy Daniela; Bonanno, Anna; Gagliardo, Rosalia; Profita, Mirella

doi:10.1016/j.imbio.2015.02.005

Cited by 77 publications

(79 citation statements)

References 33 publications

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“…Elevated sST2 levels in allergic asthmatics suggest localized production of sST2 within the airways that may act as an inhibitor of IL-33-induced inflammation. This has been demonstrated in cases of sepsis and asthma exacerbation [36, 39, 40]. …”

Section: Discussionmentioning

confidence: 98%

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IL-33 and Its Receptor ST2 after Inhaled Allergen Challenge in Allergic Asthmatics

Mitchell

Salter

Oliveria

et al. 2018

Int Arch Allergy Immunol

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Background: Previous murine models have demonstrated interleukin (IL)-33 to be an important mediator of type-2 inflammation and to promote airway hyperresponsiveness in allergic asthma. A number of inflammatory cells produce IL-33 and eosinophils express ST2 mRNA. The relationship between IL-33 and eosinophils in allergic asthma, however, remains unclear. Objective: The aim of this work was to evaluate in vitro the effect of allergen inhalation on IL-33 levels and expression of its receptor (ST2L) on eosinophils in allergic asthmatics, and the effect of IL-33 stimulation on eosinophil activity. Methods: Plasma and sputum IL-33, soluble ST2 (sST2) levels, and ST2L expression on eosinophils were measured in 10 healthy controls and 10 allergic asthmatics. Asthmatics underwent allergen and diluent inhalation challenges. Blood and sputum samples were collected to measure IL-33, sST2, and ST2L eosinophil expression before and 24 h after allergen inhalation. Purified blood eosinophils from allergic asthmatics were incubated overnight with IL-33 to assess ST2 and intracellular IL-5 expression. Results: Baseline levels of IL-33 in sputum and sST2 in plasma and sputum were similar in allergic asthmatics compared to healthy controls. In addition, there was no difference in blood or sputum eosinophil ST2L expression in healthy controls versus allergic asthmatics. Eosinophil ST2L expression was significantly increased 24 h postallergen inhalation in allergic asthmatics. In vitro stimulation of human eosinophils with IL-33 and LPS significantly increased eosinophil ST2L expression and IL-33 stimulation increased intracellular IL-5 expression, which was attenuated by treatment with sST2 and ST2 blockade. Conclusion and Clinical Relevance: In mild asthmatics, there was a significant upregulation of ST2 surface expression on eosinophils from blood and sputum following allergen inhalation challenge. In vitro, IL-33 stimulation of eosinophils increases both ST2 membrane expression and IL-5 production. These results support a role for IL-33 in causing allergen-induced eosinophilia. Blockade of IL-33 and ST2 signaling may present a novel therapeutic avenue for asthma treatment.

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Section: Discussionmentioning

confidence: 98%

“…IL-33 and sST2 has been previously shown to be increased in the peripheral blood and airways of asthmatic patients [21, 35, 36]. The principal source of IL-33 in allergic disease is not fully known; however, airway epithelial cells, smooth muscle cells, and mast cells have been identified as key sources [18, 19, 37, 38].…”

Section: Discussionmentioning

confidence: 99%

IL-33 and Its Receptor ST2 after Inhaled Allergen Challenge in Allergic Asthmatics

Mitchell

Salter

Oliveria

et al. 2018

Int Arch Allergy Immunol

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“…Such events can conclude with the more severe symptoms of allergy, such as asthma, rhinitis, dermatitis, and less frequently systemic anaphylaxis. Additionally, recently identified cytokines such as IL-25, thymic stromal lymphopoietin (TSLP), and IL-33, secreted by injured epithelial cells among others, have been associated with the development of the Th2 response (78, 79). Furthermore, additional T-cell subsets contribute to the allergic airway disease, such as IL-9-producing Th9 cells but also Th1 and Th17 cells (80).…”

Section: Immune Maturation and Allergy/asthma Incidencementioning

confidence: 99%

Regulatory T Cells in Allergy and Asthma

2017

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The immune system’s correct functioning requires a sophisticated balance between responses to continuous microbial challenges and tolerance to harmless antigens, such as self-antigens, food antigens, commensal microbes, allergens, etc. When this equilibrium is altered, it can lead to inflammatory pathologies, tumor growth, autoimmune disorders, and allergy/asthma. The objective of this review is to show the existing data on the importance of regulatory T cells (Tregs) on this balance and to underline how intrauterine and postnatal environmental exposures influence the maturation of the immune system in humans. Genetic and environmental factors during embryo development and/or early life will result in a proper or, conversely, inadequate immune maturation with either beneficial or deleterious effects on health. We have focused herein on Tregs as a reflection of the maturity of the immune system. We explain the types, origins, and the mechanisms of action of these cells, discussing their role in allergy and asthma predisposition. Understanding the importance of Tregs in counteracting dysregulated immunity would provide approaches to diminish asthma and other related diseases in infants.

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“…[9][10] A number of studies supported that either an inappropriate function Th17 cells or increased levels of Th17-related cytokines were involved in pathologic mechanism among children with AS or AR alone. [11][12] However, few studies have explored whether there were differences existing in Th17 cells immunity among children with both AS and AR. Therefore, in present…”

Section: -6mentioning

confidence: 99%

Comparison of Th17 cells mediated immunological response among asthmatic children with or without allergic rhinitis

2018

Asian Pac J Allergy Immunol

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Objective: To investigate whether there were differences in Th17 cells mediated immunological responses among asthmatics with or without allergic rhinitis. Methods:A case-control comparison was conducted in a cohort of 67 children with asthma (AS), 50 children with allergic rhinitis (AR), 52 children with both AS and AR (ASR), 25 infectious rhinitis (IR), and 55 healthy controls (HC). The percentages of circulating Th17 cells were determined by flow cytometry. The Th2-and Th17-related cytokines in plasma and culture supernatants were measured by enzyme-linked immunosorbent assay. The effect of proinflammation cytokine IL-17E on Th2 cytokines production from human T helper (Th) lymphocytes was analyzed. Conclusion:Our findings preliminarily revealed that Th17 cell and its related cytokines might be involved in pathogenesis of airway inflammation diseases, and also presenting varying immunological characteristics among asthmatic children with or without allergic rhinitis.

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IL-33/ST2 axis controls Th2/IL-31 and Th17 immune response in allergic airway diseases

Cited by 77 publications

References 33 publications

IL-33 and Its Receptor ST2 after Inhaled Allergen Challenge in Allergic Asthmatics

IL-33 and Its Receptor ST2 after Inhaled Allergen Challenge in Allergic Asthmatics

Regulatory T Cells in Allergy and Asthma

Comparison of Th17 cells mediated immunological response among asthmatic children with or without allergic rhinitis

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