02051nas a2200301 4500000000100000008004100001260001300042653001400055653002000069653003800089653001100127653001900138653001200157653002200169653002600191653003200217100001300249700001400262700002000276700001400296245004200310856005100352300001200403490000700415050003200422520128100454022001401735 2006 d c2006 Sep10aCytokines10aGenetic Markers10aGenetic Predisposition to Disease10aHumans10aInterleukin-1010aleprosy10aLymphotoxin-alpha10aReceptors, Calcitriol10aTumor Necrosis Factor-alpha1 aMoraes M1 aCardoso C1 aVanderborght PR1 aPacheco A00aGenetics of host response in leprosy. uhttps://leprosyreview.org/article/77/3/18-9202 a189-2020 v77 aInfolep Library - available3 a
In this review, we discuss recently accumulated data, analysing genetic influence on leprosy outcome. Most leprosy-related epidemiological studies are based on the comparison of frequencies of genetic markers in case-control designs using candidate genes, mainly on immunological pathways. Genomic scans using family-based designs also identified some chromosome regions to be tested for association with leprosy. The results have suggested that different genes are implicated in resistance/susceptibility to leprosy, such as tumour necrosis factor-alpha (TNFalpha), interleukin (IL)-10, vitamin D receptor (VDR), and parkin, although some of the results obtained in different populations are controversial. In spite of the recent advances in genomics and genetic epidemiology we have experienced, the results must be confirmed using better designed epidemiological studies to directly pinpoint the genes responsible for leprosy outcome. Furthermore, there is a clear requirement of functional/biological data in order to validate epidemiological findings. In this way, these genetic markers could be used to screen high-risk populations introducing gene testing as diagnostic and prognostic tools to interrupt the chain of transmission and prevent neurological damage.
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