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. 2018 Sep 6;8:13351. doi: 10.1038/s41598-018-31569-1

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© The Author(s) 2018

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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Inhibition of prostaglandin synthesis restores both lymphocyte proliferation and activation. Cardiosphere-derived cells (CDCs) were co-cultured with lymph node cells (LNCs) in the presence of ConA at a ratio of 1:10 (CDC:LNC). The addition of indomethacin (20 µM), a cyclooxygenase inhibitor, significantly increased the proliferation of LNCs; independent of donor and recipient cell line (n = 3, p < 0.05, a and b). a and b are biological replicates with technical triplicates in each, bars represent mean ± SEM of the technical replicates. CD25 signal intensity was also more when indomethacin was added to co-culture of CDCs and LNCs in the presence of ConA compared to when no indomethacin is added (n = 3, p < 0.001, c–f). The percentage of cells expressing CD25 was also partially restored by the addition of indomethacin (n = 3, p < 0.001, g). Bars represent mean ± SEM of 3 dogs.