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Front. Immunol. | doi: 10.3389/fimmu.2018.02694


 Benjamin P. Hurrell1, Pedram Shafiei Jahani1 and  Omid Akbari1*
  • 1Keck School of Medicine of USC, University of Southern California, United States

Allergic diseases including asthma, chronic rhinosinusitis and atopic dermatitis are common conditions worldwide. While type 2 immune responses induced by T-cells significantly cause allergic inflammation, the recently identified group two innate lymphoid cells (ILC2s) are emerging as critical players in the development of allergy. Upon allergen exposure, ILC2s are rapidly activated by cytokines released by epithelial cells. Activated ILC2s release various effector cytokines altogether contributing to the pathogenesis of allergy and can even cause inflammation in the absence of T-cells, as observed in asthma. Although the factors inducing ILC2 activation have been identified, evidence suggests that multiple factors can enhance or repress ILC2 proliferation, trafficking or secretion of effector cytokines upon allergic inflammation. In this review, we discuss the recent findings that influence ILC2 activation and the resulting effects on the pathogenesis of allergy. A better understanding of how ILC2s are modulated will open the door to the development of new therapeutic strategies against allergic diseases.

Keywords: ILC2, allergic disease, Asthma, activation, inhibition

Received: 21 Sep 2018; Accepted: 31 Oct 2018.

Edited by:

Clinton Mathias, Western New England University, United States

Reviewed by:

Dominique M. Bullens, KU Leuven, Belgium
Lauren A. Zenewicz, University of Oklahoma Health Sciences Center, United States  

Copyright: © 2018 Hurrell, Shafiei Jahani and Akbari. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Omid Akbari, Keck School of Medicine of USC, University of Southern California, Los Angeles, United States,