@article{22259,
  keywords = {Case-Control Studies, Cohort Studies, Cytokines, Genetic Predisposition to Disease, Genetic Variation, Haplotypes, Host-Pathogen Interactions, Humans, India, leprosy, Linkage Disequilibrium, Logistic Models, Mycobacterium leprae, Polymorphism, Single Nucleotide, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization},
  author = {Aggarwal S and Ali S and Chopra R and Srivastava AK and Kalaiarasan P and Malhotra D and Gochhait S and Garg V and Bhattacharya S N and Bamezai R},
  title = {Genetic variations and interactions in anti-inflammatory cytokine pathway genes in the outcome of leprosy: a study conducted on a MassARRAY platform.},
  abstract = {<p><b>BACKGROUND: </b>Mycobacterium leprae is the etiologic pathogen that causes leprosy. The outcome of disease is dependent on the host genetic background.</p><p><b>METHODS: </b>We investigated the association of 51 single-nucelotide polymorphisms (SNPs) in anti-inflammatory cytokines (IL-10, TGFB1, IL-6, IL-4, and IL-13) and receptors (IL-10RA, IL-10RB, TGFBR1, TGFBR2, IL-6R, IL-4R, IL-5RA, IL-5RB, and IL-13RA1) with susceptibility to leprosy in a case-control study from New Delhi in northern India. This was followed by replication testing of associated SNPs in a geographically distinct and unrelated population from Orissa in eastern India. The functional potential of SNPs was established with in vitro reporter assays.</p><p><b>RESULTS: </b>Significant associations (P < .05) were observed for 8 polymorphisms (rs1800871, rs1800872, and rs1554286 of IL-10; rs3171425 and rs7281762 of IL-10RB; rs2228048 and rs744751 of TGFBR2; and rs1800797 of IL-6) with leprosy. This association was replicated for 4 SNPs (rs1554286 of IL-10, rs7281762 of IL-10RB, rs2228048 of TGFBR2, and rs1800797 of IL-6). The interaction study revealed a significantly greater association with leprosy risk than was obtained for any SNP individually.</p><p><b>CONCLUSIONS: </b>This study provides an interesting insight on the cumulative polygenic host component that regulates leprosy pathogenesis.</p>},
  year = {2011},
  journal = {The Journal of infectious diseases},
  volume = {204},
  pages = {1264-73},
  month = {2011 Oct 15},
  publisher = {Oxford University Press},
  address = { Oxford },
  issn = {1537-6613},
  doi = {10.1093/infdis/jir516},
  language = {eng},
}