02069nas a2200349   4500000000100000008004100001260001300042653002800055653002500083653001900108653003800127653001100165653001000176653003100186653001200217653002600229653003000255653001700285100001400302700001100316700001200327700001600339700001200355700001300367700001400380700001200394245007700406300001000483490001500493520119700508022001401705       2007                            d  c2007 Apr10a3' Untranslated Regions10aCase-Control Studies10aCohort Studies10aGenetic Predisposition to Disease10aHumans10aIndia10aInterleukin-12 Subunit p4010aleprosy10aPolymorphism, Genetic10aPromoter Regions, Genetic10aTuberculosis1 aMorahan G1 aKaur G1 aSingh M1 aRapthap C C1 aKumar N1 aKatoch K1 aMehra N K1 aHuang D00aAssociation of variants in the IL12B gene with leprosy and tuberculosis.  a234-60 v69 Suppl 13 a<p>There is a great range in outcomes after mycobacterial infections, and this is probably due to individual variation in immune responses. One of the key cytokine regulators of the immune response is interleukin (IL-) 12. The IL12B gene encodes the p40 chain of both IL-12 and IL-23 and it has two major variant sites at which different alleles are associated with increased levels of gene expression and with susceptibility to a range of immune-related diseases. We hypothesized that IL12B variants associated with increased expression would be as associated with susceptibility to persistent mycobacterial infection. We tested this hypothesis by genotyping Indian subjects, having either leprosy or tuberculosis (TB), as well as ethnically matched controls. Subjects with leprosy were less likely to have the 3'UTR genotype associated with lower IL12B expression (P= 0.001). Subjects with TB were not only more likely to have the high-expressing IL12B promoter genotype (P= 0.01) but also more likely to have this in the same haplotype with the high expressing 3'UTR allele (P= 0.0009). These results suggest these infectious diseases may be improved by modulating IL-l2p40 production.</p>  a0001-2815