Role of Group 2 Innate Lymphocytes in Aspirin-exacerbated Respiratory Disease Pathogenesis

Overview

Journal Am J Rhinol Allergy

Publisher Sage Publications

Specialties Allergy & Immunology
Otorhinolaryngology

Date 2018 Jan 17

PMID 29336282

Citations 12

Authors

Andrew A White

Taylor A Doherty

Affiliations

Soon will be listed here.

Abstract

Aspirin-exacerbated respiratory disease (AERD) is characterized by chronic eosinophilic nasal polyps, asthma, and airway reactions upon cyclooxygenase (COX) 1 inhibition. AERD is present in up to 7% of adult patients with asthma and the underlying pathogenesis remains largely elusive but prostaglandin D2, cysteinyl leukotrienes, mast cells, and type 2 cytokines are thought to contribute. A wealth of studies have recently implicated group 2 innate lymphoid cells (ILC2), a novel lineage-negative lymphocyte population that produces type 2 cytokines, in human allergic disease pathogenesis. Importantly, our recent work identified that ILC2s are recruited to the nasal mucosa of patients on AERD after COX-1 inhibitor administration. Here, we review the potential impact of ILC2s in the development and propagation of type 2 inflammation in AERD.

Citing Articles

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Espuela-Ortiz A, Martin-Gonzalez E, Poza-Guedes P, Gonzalez-Perez R, Herrera-Luis E Genes (Basel). 2023; 14(9).

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Phenotype overlap in the natural history of asthma.

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Metabolic regulation by prostaglandin E impairs lung group 2 innate lymphoid cell responses.

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Biomarkers for predicting response to long-term high dose aspirin therapy in aspirin-exacerbated respiratory disease.

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