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. 2022 May 27;13:857954. doi: 10.3389/fimmu.2022.857954

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Copyright © 2022 Sasaki, Kato, Hemmi, Fukuda-Ohta, Wakaki-Nishiyama, Yamamoto and Kaisho

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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Crosstalk between XCR1+ DC and intestinal T cells. (A) Immunofluorescence imaging of intestinal sections from XCR1-Venus (Xcr1^+/venus ) mice. XCR1+ DC can be detected by Venus expression. Cell nuclei were stained with Diamidino-2-phenylindole. (B) Once activated, intestinal T cells produce XCL1, which attracts XCR1+ DC. XCR1+ DC support survival, upregulation of CD103, CCR9, α4β7, and XCL1 expression, downregulation of CD62L expression and generation of CD4+CD8αα+ IEL, thereby leading to maintenance of intraepithelial and LP T cell populations. T cell-derived XCL1 then keep CCR7 expression of XCR1+ DC to enable migration of XCR1+ DC from the LP to the mesenteric lymph nodes. High expression of XCR1 and β8 integrin and high activity of aldehyde dehydrogenase, which can convert retinal to retinoic acid, contribute to XCR1+DC-dependent mechanisms.