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. 2021 Jun 21;12:685559. doi: 10.3389/fimmu.2021.685559

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Copyright © 2021 Li, Steiger, Fei, Li, Shi, Salei, Schraml, Zheng, Anders and Lichtnekert

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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Absence of type I conventional dendritic cells (cDC1s) delays tubular recovery after IRI. IRI was induced in Irf8-deficient mice (Irf8 ^fl/fl Clec9a ^cre mice) and control mice (Irf8 ^fl/fl Clec9a ^wt mice). (A) Intrarenal mRNA expression of the regeneration genes interleukin-10 (Il-10) and Il-22 in mice in healthy state and after IRI (n = 3–6 mice/group). Representative pictures of (B) Lotus tetragonolobus lectin (Lectin)-stained kidney sections for proximal tubule (Bars = 100 μm) and (C) Tamm-Horsfall protein (THP)-stained kidney sections for distal tubule (Bars = 50 μm) in healthy mice and 7 days after IRI. Quantitative assessment of living tubule per kidney (n = 3–5 mice/group). Data are means ± SD. Two-way ANOVA test. ^* P < 0.05; ^***P < 0.001.