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Journal of Experimental Nephrology

ISSN: 2767-3383

Commentary Open Access
Volume 1 | Issue 1 | DOI: https://doi.org/10.46439/nephrology.1.002

Toll-like receptor 3 signaling and human glomerular endothelial cells

Hiroshi Tanaka1,2, Tadaatsu Imaizumi3
  • 1Department of School Health Science, Hirosaki University Faculty of Education, Hirosaki, 036-8560 Japan
  • 2Department of Pediatrics, Hirosaki University Hospital, Hirosaki, 036-8563 Japan
  • 3Department of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki, 036-8562 Japan
+ Affiliations - Affiliations

Corresponding Author

Hiroshi Tanaka, hirotana@hirosaki-u.ac.jp

Received Date: June 21, 2020

Accepted Date: July 01, 2020

Citation:

Tanaka H, Imaizumi T. Tolllike receptor 3 signaling and human glomerular endothelial cells. J Exp Nephrol 2020; 1(1):9-11.


Copyright: © 2020 Tanaka H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Given that viral infections may trigger either the development of inflammatory renal disease or the worsening of pre-existing renal disease, activated signaling through Toll-like receptor 3 (TLR3) reportedly plays a role in the pathogenesis of glomerular diseases (GN). Concerning TLR3 in intrinsic glomerular cells, it has been reported that the activation of TLR3 and downstream immune responses can be induced by both infectious organisms and endogenous ligands and leading to the development of “pseudo” antiviral immunity-related inflammations in the kidney. Therefore, this theory is probably involved in the pathophysiology of GN, especially in lupus nephritis (LN). Glomerular endothelial cells (GECs) are directly exposed to circulating viral particles in the glomerulus. Thus, the specific molecular mechanisms underlying the initiation of glomerular inflammation thorough the activation of endothelial TLR3 signaling need to be determined. We found that endothelial TLR3 activation leads to inflammatory chemokine and adhesion molecule expression in human GECs. We believe that elucidating the specific mechanisms of human endothelial TLR3 signaling in GECs will assist in the development of possible curative strategies for GN, particularly in LN in the future.

Keywords

Chloroquine, Glomerular endothelial cells, Lupus nephritis, Pseudoviral immunity, Toll-like receptor 3

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