Mesangial Viral and Psuedoviral Immunity: Possible Involvement in the Pathogenesis of Pediatric-Onset Active Lupus Nephritis
|Hiroshi Tanaka1,2* and Tadaatsu Imaizumi3|
|1Department of School Health Science, Faculty of Education, Hirosaki University, Hirosaki, Japan|
|2Department of Pediatrics, Hirosaki University Hospital, Hirosaki, Japan|
|3Department of Vascular Biology, Graduate School of Medicine, Hirosaki University, Hirosaki, Japan|
|Corresponding Author :||Hiroshi Tanaka
MD, PhD, Department of School Health Science
Faculty of Education, Hirosaki University, Hirosaki, 036-8650 Japan
E-mail: [email protected]
|Received: November 22, 2015 Accepted: December 18, 2015 Published: December 25, 2015|
|Citation: Tanaka H, Imaizumi T (2015) Mesangial Viral and Psuedoviral Immunity: Possible Involvement in the Pathogenesis of Pediatric-Onset Active Lupus Nephritis . J Arthritis 4:183. doi:10.4172/2167-7921.1000183|
|Copyright: © 2015 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.|
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Background: Since viral infections activate type I interferon (IFN) pathways and cause subsequent release of IFN-dependent proinflammatory chemokines/cytokines, the innate immune system plays an important role in the pathogenesis of lupus nephritis (LN) as well as systemic lupus erythematosus. With respect to this issue, mesangial chemokine/cytokine expressions via innate immunity reportedly play a pivotal role in the pathogenesis of LN. Also, it has been reported that pediatric-onset active LN is found as having more severe acute inflammation than that of adult cases. Therefore, viral or “pseudoviral” infections may be attributable, at least in part, to the pathogenesis of LN, especially in pediatric-onset cases.
Methods: So far, we have examined the toll-like receptor (TLR) 3 signaling cascades treated with polyinosinicpolycytidylic acid (poly IC), a synthetic analogue of viral dsRNA, that makes “pseudoviral” infection in cultured human mesangial cells (MCs).
Results: We found that the activation of mesangial TLR3 upregulated the expression of functional molecules acting as monocyte/macrophage and lymphocyte chemoattractants in MCs. Further, intense glomerular expressions of these functional molecules were observed in biopsy specimens from children with active LN.
Conclusion: These observations further support the implication of viral and “pseudoviral” immunity in the pathogenesis of active LN, especially in pediatric-onset cases.