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. 2020 Nov 16;11:554880. doi: 10.3389/fimmu.2020.554880

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Copyright © 2020 Wu and Shen

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.

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The plasticity of innate lymphoid cells (ILCs) contributes to Crohn’s disease (CD). In a healthy state, NCR⁺type3 ILC form the majority of ILCs in the lamina propria of the intestine. IL-22 is then produced, which is important for tissue regeneration and the secretion of mucous, antimicrobial peptides (AMPs) and IL-10. In the inflamed intestine of CD patients, the majority of ILCs has a type1 ILC phenotype and produce IFN-γ and TNF. The plasticity of type 2 ILCs and type 3 ILCs, allowing trans-differentiation into type 1 ILCs involved in the pathogenesis of intestinal inflammatory diseases such as CD. Under the influence of IL-12 and IL-2 regulated by DCs, the differentiation of type 3 ILCs to type 1 ILCs increases. In addition, under the action of IL-12, type 2 ILCs can also be converted into type 1 ILCs. Type 1 ILCs, before and after transformation, jointly promoted the increase of interferon (IFN)-γ production. This transformation is reversible, and type 1 ILCs can revert to type 3 ILCs in the presence of IL-23, IL-1β, and retinoic acid (RA) secreted by DCs.