Role of Group 2 Innate Lymphocytes in Aspirin-exacerbated Respiratory Disease Pathogenesis. Issue 1 (January 2018)

• Record Type: Journal Article
• Authors: White, Andrew A.; Doherty, Taylor A.
• Is Part Of: American journal of rhinology & allergy. Volume 32:Issue 1(2018)
• Page Start: 7
• Page End: 11
• Publication Date: 2018-01
• Subjects: Nose -- Periodicals; Allergy -- Periodicals; 616.21005
• DOI: 10.2500/ajra.2018.32.4498
• Languages: English
• ISSNs: 1945-8924

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.