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Nucleic acids of mammalian origin can act as endogenous ligands for Toll-like receptors and may promote systemic lupus erythematosus - Franck J. Barrat Ph.D.

October 17, 2005

After the discovery of the protein Toll as a signaling receptor for immunity in Drosophila melanogaster,several homologous Toll-like receptors (TLRs) have been identified in mammals. TLRs are key receptors of the innate immune system and recognize a diverse range of conserved microbial molecules (1, 2). 4 out of the 10 TLRs identified in humans recognize nucleic acids, demonstrating the fundamental importance of microbial DNA and RNA in triggering innate responses to pathogenic microorganisms (3–6). TLR-mediated activation can initiate rapid and effective control of infection; however, the consequences to the host can be chronic or acute inflammation. Microbial sepsis is the best known example of this, and the roles of TLR2 and TLR4 in sepsis have been clearly demonstrated (7). TLR3 has recently been shown to be required for the central nervous system inflammation leading to the disruption of the blood–brain barrier during West Nile virus infection in mice (8). This demonstrates that the nucleic acid component of a pathogen, in this example an RNA virus, can trigger inflammation destructive to host tissues. In addition, TLR activation by endogenous ligands has been reported in some types of sterile inflammation as well (9, 10).


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Source: Alliance for Lupus Research
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