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. 2020 Jun 5;8:398. doi: 10.3389/fcell.2020.00398

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Copyright © 2020 Lei, Ehle, Kumar, Müller, Moll, Malone, Humphreys, Andrassy and Anders.

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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Par2 deficiency in grafts attenuated renal allograft rejection in vivo. (A) Experimental design. Wild-type Balb/c kidneys (syngeneic) or wild-type C57BL/6 (allogeneic) were transplanted to wild-type Balb/c mice. Par2-deficient kidneys from C67BL/6 background (allogeneic) were transplanted into wild-type Balb/c mice. At day 10 after transplantation, mice were sacrificed for analysis. (B) Histological score for mouse kidney grafts. Tubulitis, intimal arteritis, glomerulitis, and interstitial inflammation were quantified by the Banff scoring method. **p < 0.01 B6 to Balb/c vs. Balb/c to Balb/c, ***p < 0.001 B6 to Balb/c vs. Balb/c to Balb/c, ^#p < 0.05 B6 to Balb/c vs. Par2KO to Balb/c. N = 4 for Balb/c to Balb/c, n = 4–6 for B6 to Balb/c, n = 6 for Par2KO to Balb/c. (C) Proinflammation gene expression in mouse kidney grafts by RT-qPCR. (D) Cd4 and Cd8b1 gene expression in mouse kidney grafts. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. B6 represents for C56BL/6J. Par2KO represent for Par2 deficiency.