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. 2017 Nov 6;7:14517. doi: 10.1038/s41598-017-15160-8

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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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Putative mechanism of auto antibody mediated human mesangial cell induced inflammation and aberrant miRNA downstream regulation. In the early phase, auto antibodies (Ab) attach to chromatin structure or membrane antigens on human mesangial cell (HMC) membranes inducing complement fixation. The miR-10a is downregulated and enhances cell proliferation or apoptosis through HOXA1, KLF4, and CREB1. IL8 or CXCL8 are putative direct targets of miR-10a. The IL-8 attracts phagocytes into the kidney. HMCs interact with endothelial cells and the glomerular basement membrane, and abnormal functions of HMCs might disturb other resident kidney cell functions. The increase in HMC number might increase mesangial matrixes resulting in chromatin or apoptotic body accumulation. In summary, these processes might drive the progression of lupus nephritis (LN) disease and provide insights into LN pathogenesis.