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. 2019 Feb 14;9:2038. doi: 10.1038/s41598-018-38432-3

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© The Author(s) 2019

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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Blockage of IFNγ ameliorated NTN in PD-L1^−/− mice. PD-L1^−/− mice received i.p. an anti-IFNγ antibody or the respective isotype control and were analyzed 8 days after induction of NTN. (A) Crescent formation was quantified in PAS-stained kidney sections of anti-IFNγ antibody-treated nephritic PD-L1^−/− mice and isotype-treated nephritic PD-L1^−/− and WT mice. (B) Albumin-creatinine-ratio was determined in urine by ELISA. (C) Renal mRNA expression of anti-IFNγ antibody- and isotype-treated nephritic PD-L1^−/− mice was analyzed by quantitative real-time RT-PCR and normalized to mRNA expression of isotype-treated nephritic WT mice. (D) Frequencies of renal CD4⁺ T cells and IFNγ-expressing CD4⁺ T cells were analyzed by flow cytometry. Representative dot plots are depicted. Mean ± SEM of one experiment out of two experiments with 4 mice per group are shown. *p < 0.05; **p < 0.01; ns, not significant; Il12b: IL-12 subunit p40; Tbx21: T-bet.