Toll-like receptors revisited; a possible role for TLR1 in lupus nephritis

Because of sinusitis and interstitial pneumonitis confirmed by chest tomography, the patient received doxycycline, and the fever and cough slowly disappeared, as did rash. Growing evidence highlights the role of podocytes in LN, not only as an integral part of kidney filtration barrier, but also their active involvement in immune-mediated kidney injury.5 Podocytes constitutively express TLR1–6 and TLR8, respond to TLR ligands with proinflammatory cytokine release, activation of type I IFN signalling, and, ultimately, podocyte injury with proteinuria.6 While innate immune responses play a central role in podocyte injury, evidence suggests that podocyte injury can initiate kidney damage in LN.5 We identified a rare variant associated with LN, which affects TLR1 gene expression and might exert its effect via podocytes and immune cells. [...]exogenous TLR ligands might contribute to the development of LN, rare polymorphisms in this locus might be considered when treating patients with LN triggered by exogenous agents.