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. 2021 Feb 17;385(2):281–292. doi: 10.1007/s00441-020-03403-6

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Intestinal microbiota-induced T_H17 cells egress from the gut dependent on S1PR1 into the circulation, in this way serving as an intestinal T_H17 cell “reservoir” and infiltrate the kidney via chemokine receptor CCR6 to mediate kidney damage in crescentic glomerulonephritis. CCR, CC-chemokine receptor; S1PR, sphingosine 1-phosphate receptor