Implication of the expression of retinoic acid-inducible gene-I in human glomerulonephritis

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Viral infections may trigger the development of inflammatory renal disease or the worsening of pre-existing renal disease. Viral double-stranded RNA (dsRNA) can activate not only toll-like receptors (TLR) 3 located within intracellular endosomes and 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 non-infectious stimuli such as endogenous ligands, and this mechanism may be involved in the pathogenesis of autoimmune renal diseases. Based on our recent experimental studies using cultured normal human mesangial cells (MCs), we found that novel TLR3/RIG-I-mediated signaling pathways in MCs may be involved in the pathogenesis of glomerular diseases.