4.5 Article

Lipid mediators as regulators of human ILC2 function in allergic diseases

Journal

IMMUNOLOGY LETTERS
Volume 179, Issue -, Pages 36-42

Publisher

ELSEVIER
DOI: 10.1016/j.imlet.2016.07.006

Keywords

Innate lymphoid cells; Asthma; Atopic dermatitis; Prostaglandins; Leukotrienes; Lipoxins

Categories

Funding

  1. European Union's Horizon research and innovation program under the Marie Sklodowska-Curie grant [655677]
  2. Austrian Science Fund FWF [P25531-B23]
  3. Swedish Research Council
  4. Swedish Society for Medical Research
  5. Austrian Science Fund (FWF) [P25531] Funding Source: Austrian Science Fund (FWF)
  6. Marie Curie Actions (MSCA) [655677] Funding Source: Marie Curie Actions (MSCA)

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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. (C) 2016 The Author(s). Published by Elsevier B.V. on behalf of European Federation of Immunological Societies. This is an open access article under the CC BY-NC-ND license.

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