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Lipid mediators as regulators of human ILC2 function in allergic diseases.
- Source :
-
Immunology letters [Immunol Lett] 2016 Nov; Vol. 179, pp. 36-42. Date of Electronic Publication: 2016 Jul 07. - Publication Year :
- 2016
-
Abstract
- Group 2 innate lymphoid cells (ILC2) are specialized in type 2 immunity. ILC2 are activated early in immune responses and, despite their low abundance, are able to initiate and amplify allergic inflammation by orchestrating other type 2 immune cells. Based on recent discoveries, the spectrum of ILC2 regulating factors has been extended. It is now well established that not only epithelial cell-derived innate cytokines, but also bioactive lipids can regulate ILC2 activity and accumulation. Additionally, ILC2 appear to be susceptible to changes in the cytokine milieu and can acquire an ILC1-like phenotype due to a high degree of cellular plasticity. As ILC2 are fundamentally involved in the pathogenesis of type 2 diseases, they represent a promising therapeutic target for allergic airway and skin diseases. In this review we summarize the current knowledge about ILC2 biology in the allergy context, with a particular focus on the emerging role of lipid mediators in regulating ILC2 function.<br /> (Copyright © 2016 The Author(s). Published by Elsevier B.V. All rights reserved.)
- Subjects :
- Anti-Asthmatic Agents pharmacology
Anti-Asthmatic Agents therapeutic use
Cell Plasticity immunology
Humans
Hypersensitivity drug therapy
Hypersensitivity genetics
Leukotrienes metabolism
Lipoxins metabolism
Lymphocyte Subsets cytology
Lymphocyte Subsets drug effects
Molecular Targeted Therapy
Prostaglandins metabolism
Hypersensitivity immunology
Hypersensitivity metabolism
Immunity, Innate drug effects
Inflammation Mediators metabolism
Lipids
Lymphocyte Subsets immunology
Lymphocyte Subsets metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1879-0542
- Volume :
- 179
- Database :
- MEDLINE
- Journal :
- Immunology letters
- Publication Type :
- Academic Journal
- Accession number :
- 27396531
- Full Text :
- https://doi.org/10.1016/j.imlet.2016.07.006