Inflammatory Chemokine Expression via Toll-Like Receptor 3 Signaling in Normal Human Mesangial Cells
The innate and adaptive immune systems have been reported to play an important role in the pathogenesis of glomerular diseases. Since viral infections may trigger the development of inflammatory renal disease or the worsening of preexisting renal disease, recent studies have focused on the involveme...
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| Format: | Article |
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Wiley
2013-01-01
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| Series: | Clinical and Developmental Immunology |
| Online Access: | http://dx.doi.org/10.1155/2013/984708 |
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| author | Hiroshi Tanaka Tadaatsu Imaizumi |
| author_facet | Hiroshi Tanaka Tadaatsu Imaizumi |
| author_sort | Hiroshi Tanaka |
| collection | DOAJ |
| description | The innate and adaptive immune systems have been reported to play an important role in the pathogenesis of glomerular diseases. Since viral infections may trigger the development of inflammatory renal disease or the worsening of preexisting renal disease, recent studies have focused on the involvement of toll-like receptors (TLRs) and their signaling pathways in the inflammatory processes of glomerular cells. Viral double-stranded RNA (dsRNA) can activate not only TLR3 located within intracellular endosomes but also retinoic-acid-inducible-gene-I- (RIG-I-) like helicase receptors located within the cytosol. RIG-I and melanoma differentiation-associated gene 5 (MDA5) are members of the RNA helicase family in the cytosol, and both act as pathogen recognition receptors. The activation of TLRs and their downstream immune responses can be induced by both infectious pathogens and noninfectious stimuli such as endogenous ligands, and this mechanism may be involved in the pathogenesis of autoimmune renal diseases. However, there are few data on the interaction between TLR3, MDA5, and RIG-I in autoimmune glomerular diseases. Based on our recent experimental studies using cultured normal human mesangial cells (MCs), we found that novel TLR3-mediated signaling pathways in MCs may be involved in the pathogenesis of glomerular diseases. In the present paper, we summarize our recent findings. |
| format | Article |
| id | doaj-art-9e576ddb46f242a7989a6aa99075f607 |
| institution | Kabale University |
| issn | 1740-2522 1740-2530 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
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| series | Clinical and Developmental Immunology |
| spelling | doaj-art-9e576ddb46f242a7989a6aa99075f6072025-02-03T06:11:15ZengWileyClinical and Developmental Immunology1740-25221740-25302013-01-01201310.1155/2013/984708984708Inflammatory Chemokine Expression via Toll-Like Receptor 3 Signaling in Normal Human Mesangial CellsHiroshi Tanaka0Tadaatsu Imaizumi1Department of School Health Science, Hirosaki University Faculty of Education, 1 Bunkyo-cho, Hirosaki 036-8560, JapanDepartment of Vascular Biology, Graduate School of Medicine, Hirosaki University, Hirosaki 036-8562, JapanThe innate and adaptive immune systems have been reported to play an important role in the pathogenesis of glomerular diseases. Since viral infections may trigger the development of inflammatory renal disease or the worsening of preexisting renal disease, recent studies have focused on the involvement of toll-like receptors (TLRs) and their signaling pathways in the inflammatory processes of glomerular cells. Viral double-stranded RNA (dsRNA) can activate not only TLR3 located within intracellular endosomes but also retinoic-acid-inducible-gene-I- (RIG-I-) like helicase receptors located within the cytosol. RIG-I and melanoma differentiation-associated gene 5 (MDA5) are members of the RNA helicase family in the cytosol, and both act as pathogen recognition receptors. The activation of TLRs and their downstream immune responses can be induced by both infectious pathogens and noninfectious stimuli such as endogenous ligands, and this mechanism may be involved in the pathogenesis of autoimmune renal diseases. However, there are few data on the interaction between TLR3, MDA5, and RIG-I in autoimmune glomerular diseases. Based on our recent experimental studies using cultured normal human mesangial cells (MCs), we found that novel TLR3-mediated signaling pathways in MCs may be involved in the pathogenesis of glomerular diseases. In the present paper, we summarize our recent findings.http://dx.doi.org/10.1155/2013/984708 |
| spellingShingle | Hiroshi Tanaka Tadaatsu Imaizumi Inflammatory Chemokine Expression via Toll-Like Receptor 3 Signaling in Normal Human Mesangial Cells Clinical and Developmental Immunology |
| title | Inflammatory Chemokine Expression via Toll-Like Receptor 3 Signaling in Normal Human Mesangial Cells |
| title_full | Inflammatory Chemokine Expression via Toll-Like Receptor 3 Signaling in Normal Human Mesangial Cells |
| title_fullStr | Inflammatory Chemokine Expression via Toll-Like Receptor 3 Signaling in Normal Human Mesangial Cells |
| title_full_unstemmed | Inflammatory Chemokine Expression via Toll-Like Receptor 3 Signaling in Normal Human Mesangial Cells |
| title_short | Inflammatory Chemokine Expression via Toll-Like Receptor 3 Signaling in Normal Human Mesangial Cells |
| title_sort | inflammatory chemokine expression via toll like receptor 3 signaling in normal human mesangial cells |
| url | http://dx.doi.org/10.1155/2013/984708 |
| work_keys_str_mv | AT hiroshitanaka inflammatorychemokineexpressionviatolllikereceptor3signalinginnormalhumanmesangialcells AT tadaatsuimaizumi inflammatorychemokineexpressionviatolllikereceptor3signalinginnormalhumanmesangialcells |