Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Regulatory ILC2 – Role of IL-10 Producing ILC2 in Asthma

Version 1 : Received: 15 September 2023 / Approved: 18 September 2023 / Online: 18 September 2023 (19:16:31 CEST)

A peer-reviewed article of this Preprint also exists.

Emami Fard, N.; Xiao, M.; Sehmi, R. Regulatory ILC2—Role of IL-10 Producing ILC2 in Asthma. Cells 2023, 12, 2556. Emami Fard, N.; Xiao, M.; Sehmi, R. Regulatory ILC2—Role of IL-10 Producing ILC2 in Asthma. Cells 2023, 12, 2556.

Abstract

Over the past two decades, a growing body of evidence observations have shown group two innate lymphoid cells (ILC2) to be critical drivers of Type 2 (T2) inflammatory responses associated with allergic inflammatory conditions such as asthma. ILC2 release copious amounts of pro-inflammatory T2 cytokines – interleukin (IL)-4, IL-5, IL-9, and IL-13. This review provides a comprehensive overview of the newly discovered regulatory subtype of ILC2 described in murine and human mucosal tissue and blood. These KLRG1+ILC2 have the capacity to produce the anti-inflammatory cytokine, IL-10. Papers compiled in this review were based on query of PubMed and Google Scholar for articles published from 2000-2023 using keywords “IL-10” and “ILC2”. Studies with topical relevance to IL-10 production by ILC2 were included. ILC2 respond to microenvironmental cues including retinoic acid (RA), IL-2, IL-4, IL-10, IL-33, as well as neuropeptide mediators such as neuromedin-U (NMU), prompting a shift towards IL-10 and away from T2 cytokine production. In contrast, TGF-β attenuates IL-10 production by ILC2. Immune regulation provided by IL-10+ILC2s holds potential significance for management of T2 inflammatory conditions. The observation of context-specific cues which alter phenotype of ILC warrants examining characteristics of ILC subsets to determine the extent of plasticity or whether the current classification of ILCs requires refinement.

Keywords

Allergic Inflammatory Disease; Asthma; Type 2 Inflammation; Interleukin-10

Subject

Medicine and Pharmacology, Immunology and Allergy

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