A functional TLR3 polymorphism mediates susceptibility to SLE in anti-Ro/SSA antibody-positive patients
(2011) Société Royale Belge de Rhumatologie — Location: Anvers (28.September.2011)
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- Abstract
- We report the association between a non-synonymous single nucleotide polymorphism in the coding region of TLR3 and systemic lupus erythematosus in two populations of Caucasian patients and controls. In particular, 60.8% of anti-Ro/SSA antibody positive patients are homozygous for the TLR3 rs3775291 G allele, compared to 47.6% of the controls (p = 0.006). Functional experiments indicate that signaling through the TLR3 major G allele results in stronger induction of interferon-induced genes, increased apoptosis in response to UV irradiation, increased release of the Ro/SSA auto-antigen, increased cell surface expression of MHC II and CD86, and increased secretion of interleukin-6 by UV-irradiated monocyte-derived dendritic cells. These results indicate that homozygosity for the rs3775291 major G allele contributes to the pathogenesis of SLE by increasing the magnitude of TLR3-dependent events that potentially lead to loss of tolerance to the Ro/SSA auto-antigen in response to UV irradiation.
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Ducreux, J., & Lauwerys, B. (2011). A functional TLR3 polymorphism mediates susceptibility to SLE in anti-Ro/SSA antibody-positive patients. Société Royale Belge de Rhumatologie, Anvers. https://hdl.handle.net/2078.5/200440