Background and aims Until nowadays, the exact aetiology of SLE (Systemic Lupus Erythematosus) is still unknown. It is currently accepted that there are several factors responsible for complex immunological disorders contributing to its development. Recent studies have shown that abnormal stimulation of innate immunity may have a great influence on the immunopathogenesis of SLE. Since TLRs (Toll-Like Receptors) are essential modulators of innate immune response, its role in SLE pathogenesis has raised great interest, particularly of those recognising nucleic acid, the main antigenic target in SLE.
Analyse the role of TLR in the pathogenesis of SLE.
Methods We look up for scienctific article comprehensively in Medline, Science Direct, PubMed, and Cochrane Database. We found 20 article based on bibliography and keywords from the database.
Results The expression of TLR7 and TLR9 in peripheral blood mononuclear cells is higher in SLE group compared to control group, while the expression of other TLR shows no difference. There is also a positive correlation between TLR9 expression and activity index and R-SLEDAI score, while TLR7 expression shows positive correlation with chronicity index. Anti-Sm autoantibodies is absent in TLR7 deficiency, while anti-dsDNA autoantibodies are absent in TLR9 deficiency. TLR7 also plays crucial role in B cell proliferation.
Conclusions TLR7 and TLR9 appears to play role in pathogenesis of SLE. However, more research need to be done to understand more about the role of TLR in pathogenesis of SLE.
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