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. 2017 Nov 9;7:15135. doi: 10.1038/s41598-017-15542-y

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© The Author(s) 2017

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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P-p38MAPK, p-ERK and p-Akt in T cell subsets of TAC- (grey) and BELA- (white) treated patients after stimulation with PMA/ionomycin. (a) p-p38MAPK (left), p-ERK (middle) and p-Akt (right) within CD4⁺CD28⁺ T cells. P-p38MAPK and p-Akt, but not p-ERK, were significantly decreased in TAC-treated patients at different time points after transplantation, in contrast to BELA-treated patients. (b) p-p38MAPK (left), p-ERK (middle) and p-Akt (right) within CD8⁺CD28⁺ T cells. P-p38MAPK and p-Akt, but not p-ERK, were inhibited when TAC was given. BELA caused an increase in p-ERK at day 360. (c) p-p38MAPK (left), p-ERK (middle) and p-Akt (right) within CD8⁺CD28⁻ T cells. Phosphorylation inhibition by TAC is comparable with CD8⁺CD28⁺ T cells. (Data are plotted as box and whiskers indicating total range; n = 20 TAC-treated patients and n = 20 BELA-treated patients) *p < 0.05, **p < 0.01, ***p < 0.001.