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Factors affecting the migration of ILC2s in allergic disease

Cellular & Molecular Immunology volume 18, pages 2069–2070 (2021)Cite this article

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It is well known that group 2 innate lymphoid cells (ILC2s) are enriched in mucosal tissues and respond to epithelial cell-derived cytokines, initiating and maintaining type 2 inflammation. Although an increased number of ILC2s has been observed at sites of allergic inflammation and during helminth infection, some studies have shown that ILC2s are largely tissue-resident cells seeded in the tissue early in life,1 suggesting that such accumulation may be due to local proliferation of ILC2s. However, other studies indicate that ILC2s are able to migrate into tissues from the circulation during inflammation.2,3,4 In this case, the mechanisms that control ILC2 accumulation in tissues and the contribution of ILC2 migration into and between tissues during allergic inflammation remain unclear.

Stier et al. showed that administration of IL-33 in mice alters the expression of chemokine receptors, including C-X-C motif chemokine receptor 4, on bone marrow ILC2 progenitors (ILC2Ps), which account for this cell translocation, while mice lacking IL-33 signaling have a significant accumulation of ILC2Ps in the bone marrow and a marked reduction in the number of ILC2s in peripheral tissues.4 In addition, exposure to exogenous IL-33 and the fungal allergen Alternaria alternata (Alt) rapidly and significantly mobilized ILC2Ps to egress from the bone marrow.4 Furthermore, using IL-13-enhanced green fluorescent protein reporter mice and elegant imaging techniques, Puttur et al. found that ILC2s exhibit amoeboid-like movement and accumulate in the extravascular tissue surrounding large blood vessels rather than alveolar capillaries during IL-33-induced lung inflammation, although ILC2s exist in relatively low numbers in the lungs under steady conditions.5 These data suggest that the rapid expansion of ILC2 numbers in the lung tissues of the mice challenged with IL-33 or Alt could result as a consequence of recruitment of ILC2Ps from the bone marrow rather than in situ proliferation of a small population of resident precursors at steady status. Therefore, it is critical to define the pathways controlling ILC2 migration to and within tissues.

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Authors and Affiliations

  1. Department of Otorhinolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing Institute of Otorhinolaryngology, Key Laboratory of Otorhinolaryngology Head and Neck Surgery, Ministry of Education, Beijing Key Laboratory of Nasal Diseases, Beijing, China

    Yan Li

  2. Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China

    Yan Li, Wei Wang & Sun Ying

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  1. Yan Li
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Correspondence to Sun Ying.

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Li, Y., Wang, W. & Ying, S. Factors affecting the migration of ILC2s in allergic disease. Cell Mol Immunol 18, 2069–2070 (2021). https://doi.org/10.1038/s41423-021-00703-x

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