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. 2017 Mar 7;8(12):878–895. doi: 10.1007/s13238-017-0379-5

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© The Author(s) 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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ILC3 functions in the lung. After receiving the danger signals from the airway epithelium upon pathogen and tumor cell invasion, DCs and macrophages release IL-1β and IL-23, which activate ILC3s. Activated ILC3s release IL-17, IL-22, IL-8, IL-2, TNF, and LTα1β2. IL-17 and IL-22 play a dual role: on the one hand, they stimulate the epithelium to produce antimicrobial peptides and proteins, and mucus-associated molecules to clear the pathogen and tumor cells to maintain homeostasis of the mucosa; on the other hand, they may aggravate the development of obesity-related asthma and COPD. IL-22-producing-ILC3s may have anti-asthma effects, whereas IL-17-producing ILC3s may participate in the pathology of asthma, especially in obesity-related asthma. IL-2 and IL-8 recruit neutrophils to the lung. LTα1β2 stimulates mesenchymal stem cells (MSCs) to express ICAM-1 and VCAM-1. These molecules participate in the formation of a tertiary lymphoid organ in the tumor. See text for details