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Toll-like receptors TLRs , a large group of proteins which recognize various pathogen-associated molecular patterns, are critical for the normal function of the innate immune system. Following their discovery many single nucleotide polymorphisms within TLRs and components of their signaling machinery have been discovered and subsequently implicated in a wide range of human diseases including atherosclerosis, sepsis, asthma, and immunodeficiency. This review discusses the effect of genetic variation on TLR function and how they may precipitate disease. The immune system is comprised of two parts, the innate and adaptive systems. The innate immune system is the first line of defense against invading organisms and is highly conserved across species. Pathogens are identified on the basis of their molecular structures by a limited repertoire of so-called pattern recognition receptors PRRs. One major family of PRRs are the Toll-like receptors TLRs , a group of type I membrane glycoproteins evolutionarily conserved from Caenorhadbitis elegans to humans [ 1 , 2 ]. The founding member of the family, Toll, was identified as a protein essential for embryonic dorsoventral polarity and the antifungal response of Drosophila [ 3 ]. TLRs are expressed on various immune cells including monocytes, dendritic cells, B cells, as well as endothelial cells [ 4 ].
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