The Association Of Tlrs With Human Disease

The prominent role of TLRs in innate and adaptive immunity predicts that functional defects in any of these receptors will have a major impact on disease susceptibility. This has motivated several genetic studies of TLR polymorphisms in humans, especially on possible associations between single nucleotide polymorphisms (SNPs) and susceptibility to disease.

Several SNPs have been reported in both 77r2 and Tlr4 that may influence the susceptibility to infectious diseases [81-83]. One TLR4 polymorphism, resulting in the amino acid substitution Asp299Gly, may be associated with increased susceptibility to Gram-negative bacterial infections, [81,84-86] and protection against atherosclerosis [87]. In a small study of leprosy patients in Korea, an Arg677Trp SNP in TLR2 was found to be associated with the lepromatous, but not the tuberculoid form of the disease [83]. The Arg677Trp mutation results in a form of TLR2 that is unable to signal, further supporting a functional link between this TLR and effective resistance to M. leprae (P-Y. Bochud, unpublished results). Recently a mutant, non-signalling, form of TLR5 that is expressed with high frequency in human populations was identified (T. Hawn, unpublished results). The presence of this allele is predicted to alter the susceptibility to infec tion with flagellated organisms. Systematic studies of the association of other TLR polymorphisms and specific diseases are currently being undertaken in a number of laboratories.

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