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. 2023 Sep 11;55(9):1885–1894. doi: 10.1038/s12276-023-01024-x

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a Migration of iNKT cells to the lungs. After developing in the thymus, iNKT cells express CXCR6, a tissue localization molecule, and migrate to the CXCL16-expressing periphery. iNKT cells accumulate in the lumen of the lung microvasculature and then enter the lung tissue when neutrophils in the lung interstitium secrete the CCR4 ligands CCL17/22 and CXCL9/13. The neutrophils, therefore, guide the iNKT cells to the source of lung injury in the interstitium. The monocyte-derived DCs (moDCs) in this area present glycolipid antigens from the lung injury source to the iNKT cells, which become activated and then remain in the interstitium. b Crosstalk between iNKT cells and other cells in the lung. iNKT cells are activated by antigens expressed by lung antigen-presenting cells (APCs), such as MoDCs, by cytokines from other cells (such as IL-12/18), and by TLR ligands (e.g., LPS). The activated iNKT cells then secrete a variety of cytokines that regulate the function of many types of neighboring cells.