@article{8648, keywords = {Antigen-Presenting Cells, Asian Continental Ancestry Group, Cell Adhesion Molecules, Genetic Predisposition to Disease, genotype, Humans, Immunity, Innate, Lectins, C-Type, Nod1 Signaling Adaptor Protein, Nod2 Signaling Adaptor Protein, Polymorphism, Single Nucleotide, Receptors, Cell Surface, Toll-Like Receptor 2}, author = {Kanazawa N and Mikita N and Li H and Nakatani Y and Ozaki M and Kosaka M and Ishii N and Nishimura H and Furukawa F}, title = {[Genetic involvement of bacterial sensor molecules in Japanese leprosy].}, abstract = {

Occurrence of new patients of leprosy, caused by Mycobacterium leprae infection, is now almost absent in Japan but is still uncontrolled in developing countries. As one factor affecting the disease development, genetic predisposition of a host has been considered to be associated. Actually, various gene mutations have been reported to be associated at two stages of the disease progression, not only establishment of the disease but also determination of the phenotype, such as lepromatous (L)-type, tuberculoid (T)-type and reversal reaction. On the basis of recent progress of the research on innate immunity, here we analyzed single nucleotide polymorphisms (SNPs) of the genes of major bacterial sensor molecules expressed in antigen-presenting cells, TLR2, DC-SIGN, NOD1 and NOD2, in Japanese leprosy patients. As a result, frequency of polymorphisms in DC-SIGN -336 showed significant difference between the leprosy patients and the healthy controls, reflecting its role in establishment of the disease. Especially, among those with a particular TLR2 -16934 genotype, frequency of the polymorphisms in DC-SIGN -336 showed significant difference between the patients and the controls, suggesting any cooperation of these SNPs.

}, year = {2009}, journal = {Nihon Hansenbyo Gakkai zasshi = Japanese journal of leprosy : official organ of the Japanese Leprosy Association}, volume = {78}, pages = {255-61}, month = {2009 Sep}, issn = {1342-3681}, language = {jpn}, }