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. 2020 Feb 6;46(5):943–953. doi: 10.1007/s00134-019-05919-0

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by-nc/4.0/.

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Fig. 5 — Proposed CCL14 mechanism. a TNFα and other inflammatory mediators are released from injured epithelium and bind to TNF receptors, leading to release of CCL14 from tubular epithelial cells. b Binding of CCL14 to CCR1 and CCR5 receptors on monocytes and T cells induces chemotaxis towards site of injury. c Monocytes differentiate into macrophages and naïve T cells differentiate into proinflammatory Th1 cells