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. 2017 Jun 8;7:3057. doi: 10.1038/s41598-017-03130-z

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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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Proposed model of IS-mediated immune dysfunction provoking endothelial damage in ESRD patients. IS, a key uremic toxin which is dramatically accumulated in patients with chronic renal dysfunction, induces secretion of TNF-α by human monocytes through the aryl hydrocarbon receptor (AhR). Upon stimulation with TNF-α, human endothelial cells predominantly produce CX3CL1, a specific chemokine ligand of CX3CR1, which is highly expressed on CD4⁺CD28⁻ T cells. ESRD patients have a markedly higher frequency of circulating cytolytic CD4⁺CD28⁻ T cells, which are significantly expanded under chronic exposure to TNF-α. These CD4⁺CD28⁻CX3CR1⁺ T cells are preferentially recruited by CX3CL1 and induce apoptosis of human endothelial cells upon TCR activation.