Abstract
Systemic lupus erythematosus is an autoimmune disease with a high morbidity and nephritis is a common manifestation. Previous studies in murine lupus models have suggest a role for Toll-like receptor 2 and 4. We examined the role of these molecules in MRL lpr mice which is one of the most established and robust murine models. We compared disease parameters in Toll-like receptor 2 or Toll-like receptor 4 deficient mice with their littermate controls. We found no difference in the severity of glomerulonephritis as assessed by histology, serum creatinine and albuminuria when Toll-like receptor 2 or Toll-like receptor 4 deficient MRLlpr mice were compared with Toll-like receptor sufficient controls. We also found similar levels of anti-dsDNA and anti-ssDNA antibodies. These results show that Toll-like receptor 2 and Toll-like receptor 4 do not play a significant role in MRLlpr mice, and therefore they may not be important in human lupus.
Highlights
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterised by involvement of many organs including skin, joints, kidneys and brain
Nephritis is not Modified by TLR2 or TLR4 Deficiency We first assessed the severity of kidney disease in cohorts of mice at 18 weeks
All mice survived to 14 weeks, though by 18 weeks two TLR2 sufficient mice had died, leaving 11 in each group for analysis
Summary
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterised by involvement of many organs including skin, joints, kidneys and brain. Toll-like receptors (TLRs) are a family of structurally related molecules that recognise pathogen-associated molecular patterns. They can be broadly divided into cell-surface receptors such as TLR2 and TLR4 recognising bacterial products, and intracellular receptors such as TLR3, TLR7, TLR8 and TLR9 recognising nucleic acids. In addition several studies using the nephrotoxic nephritis model have shown a role for TLR2 and TLR4 through a number of mechanisms [5,6,7,8] Together these data support the idea that TLRs play a role in the exacerbation of lupus by bacterial and viral infection, as can be observed clinically
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