01907nas a2200349   4500000000100000008004100001260001300042653002400055653002400079653003800103653001100141653002500152653002500177653002800202653002700230653002800257653001300285653002500298653004900323653002800372653002300400653002400423653002500447653002400472100001300496700001300509245009100522300000900613490000700622520091400629022001401543       2001                            d  c2001 Jul10aAmino Acid Sequence10aDrosophila Proteins10aGenetic Predisposition to Disease10aHumans10aLeprosy, lepromatous10aLeprosy, Tuberculoid10aLeukocytes, Mononuclear10aMembrane Glycoproteins10aMolecular Sequence Data10aMutation10aMycobacterium leprae10aPolymorphism, Single-Stranded Conformational10aReceptors, Cell Surface10aSequence Alignment10aSignal Transduction10aToll-Like Receptor 210aToll-Like Receptors1 aKang T J1 aChae G T00aDetection of Toll-like receptor 2 (TLR2) mutation in the lepromatous leprosy patients.  a53-80 v313 a<p>Toll-like receptor 2 (TLR2) is critical in the immune response to mycobacterial infections and the mutations in the TLR2 have been shown to confer the susceptibility to severe infection with mycobacteria. To define this, we screened the intracellular domain of TLR2 in 131 subjects. Groups of 45 lepromatous and 41 tuberculoid leprosy (TT) patients and 45 controls were investigated. Ten subjects among the lepromatous leprosy (LL) patients had a band variant detected by single-stranded conformational polymorphism. DNA sequencing detected a C to T substitution at nucleotide 2029 from the start codon of the TLR2. The mutation would substitute Arg to Trp at amino acid residue 677, one of the conserved regions of TLR2. In our results, the mutation was involved in only LL, not TT and control. Thus, we suggest that the mutation in the intracellular domain of TLR2 has a role in susceptibility to LL.</p>  a0928-8244