Association between Group 2 Innate Lymphoid Cells enrichment, nasal polyps and allergy in Chronic Rhinosinusitis

Miljkovic, Dijana; Bassiouni, Ahmed; Cooksley, Clare; Ou, Judy; Hauben, Ehud; Wormald, Peter John; Vreugde, Sarah

doi:10.1111/all.12440

Cited by 155 publications

(125 citation statements)

References 30 publications

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“…In fact, rhinovirus infection-induced asthma exacerbations in children were associated with elevated TSLP and CCL-11 (eotaxin-1) levels that can be noninvasively detected in nasal secretions (11). The repeated report of genetic associations of IL-33 and TSLP (12) with asthma risk is particularly interesting as TSLP, IL-25 (IL-17E) and IL-33 (13) are considered to play a role in the early commitment towards Th2 immunity and type 2 innate (ILC2) lymphocytes (14). They are considered to be recruited to the site of allergic inflammation and produce IL-4, IL-5, IL-13 and IL-6 (15).…”

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confidence: 99%

“…Little is known about ILC2s during allergic sensitization in vivo, but the role of ILC2 was demonstrated in the pathophysiology of chronic rhinosinusitis (15) with nasal polyps (14,16) and asthma exacerbation (17), also suggesting a role of ILC2 as amplifiers of type 2 cytokine-mediated inflammatory processes. In the peripheral blood, higher frequencies of ILC2 (18) and higher IL-33 levels (19) are observed in asthma patients (18).…”

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confidence: 99%

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Current and future biomarkers in allergic asthma

Zissler

Bieren

Jakwerth

et al. 2016

Allergy

107

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Diagnosis early in life, sensitization, asthma endotypes, monitoring of disease and treatment progression are key motivations for the exploration of biomarkers for allergic rhinitis and allergic asthma. The number of genes related to allergic rhinitis and allergic asthma increases steadily; however, prognostic genes have not yet entered clinical application. We hypothesize that the combination of multiple genes may generate biomarkers with prognostic potential. The current review attempts to group more than 161 different potential biomarkers involved in respiratory inflammation to pave the way for future classifiers. The potential biomarkers are categorized into either epithelial or infiltrate-derived or mixed origin, epithelial biomarkers. Furthermore, surface markers were grouped into cell-typespecific categories. The current literature provides multiple biomarkers for potential asthma endotypes that are related to T-cell phenotypes such as Th1, Th2, Th9, Th17, Th22 and Tregs and their lead cytokines. Eosinophilic and neutrophilic asthma endotypes are also classified by epithelium-derived CCL-26 and osteopontin, respectively. There are currently about 20 epithelium-derived biomarkers exclusively derived from epithelium, which are likely to innovate biomarker panels as they are easy to sample. This article systematically reviews and categorizes genes and collects current evidence that may promote these biomarkers to become part of allergic rhinitis or allergic asthma classifiers with high prognostic value.

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confidence: 99%

mentioning

confidence: 99%

Current and future biomarkers in allergic asthma

Zissler

Bieren

Jakwerth

et al. 2016

Allergy

107

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“…However, not all patients with AERD can be desensitized, and this group that fails desensitization is distinguished by their constitutive overproduction and aspirin-stimulated release of PGD 2 that correlates with the severity of airflow obstruction 6 . In addition to defining a more severe subgroup that fails aspirin desensitization, PGD 2 likely contributes to the severity through its myriad of biological activities that includes inducing vasodilation and vascular leakage, bronchoconstriction, and the recruitment and activation of basophils, eosinophils, dendritic cells, and both Th2-like lymphocytes and type 2 innate lymphoid cells [8][9][10][11] .…”

Section: Introductionmentioning

confidence: 99%

Eosinophil Production of PGD2 in Aspirin-Exacerbated Respiratory Disease

Steinke

Negri

Baker

et al. 2016

Journal of Allergy and Clinical Immunology

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Background-Aspirin-exacerbated respiratory disease (AERD) differs from aspirin tolerant disease due in part to eosinophilic tissue infiltration and over-expression of arachidonic acid metabolic pathway components that lead to enhanced secretion of cysteinyl leukotrienes (CysLT) and prostaglandin D 2 (PGD 2 ) observed constitutively and, paradoxically, in response to aspirin and other cyclooxygenase inhibitors. We have previously demonstrated the capacity of interferon (IFN)-γ to drive CysLT expression and response.

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“…Patients with chronic rhinosinusitis (CRS) and atopic dermatitis show increased levels of ILC2s in nasal polyps and skin lesions respectively [11][12][13]. Recent studies show elevated ILC2 levels in both the sputum and blood of adult severe asthmatics compared to mild asthmatics, as well as in the BAL, induced sputum, and blood of children with severe asthma compared to children without [14,15].…”

Section: Introductionmentioning

confidence: 99%

Lipid Mediator Regulation of Group 2 Innate Lymphoid Cells

MR¹,

TA²

2016

Immunome Res

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ILC2s were originally found to be activated by epithelial cell derived cytokines to induce the secretion of Th2 cytokines, IL-5 and IL-13. Recent research has shown that lipid mediators play a large role in the activation and inhibition of ILC2 function. Unlike the traditional epithelial cell derived cytokines IL-33 and IL-25, lipid mediators have been shown to promote ILC2 secretion of not only IL-5 and IL-13, but the secretion of IL-4 as well. Prostaglandin D 2 has been shown to be a potent chemoattractant of ILC2s as well as a potent activator of ILC2s to release Th2 cytokines. In addition to prostaglandin D 2 , cysteinyl leukotrienes also activate ILC2s to secrete Th2 cytokines during inflammation. Notably, lipid mediators have been shown to work in concert with epithelial cell derived cytokines to increase IL-5 and IL-13 secretion from ILC2s. On the other hand, lipid meditators prostaglandin I 2 and lipoxin A 4 are the first identified lipid mediator inhibitors of ILC2 function, and thus limit ILC2 contribution to Th2 inflammation. ILC2s play a potential significant role in Th2 mediated inflammation in a variety of allergic disease states, such as asthma, atopic dermatitis, and chronic rhinosinusitis. The identification of lipid mediators as activators and inhibitors of ILC2 function provides additional therapeutic targets for altering ILC2 function during disease states.

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Association between Group 2 Innate Lymphoid Cells enrichment, nasal polyps and allergy in Chronic Rhinosinusitis

Abstract: Our results characterize the complex interactions between ILC2s and other Th2 response elements in the context of CRS and suggest that ILC2 enrichment occurs in CRSwNP and in allergic CRS patients.

Cited by 155 publications

References 30 publications

Current and future biomarkers in allergic asthma

Current and future biomarkers in allergic asthma

Eosinophil Production of PGD2 in Aspirin-Exacerbated Respiratory Disease

Lipid Mediator Regulation of Group 2 Innate Lymphoid Cells

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