@article{7964, keywords = {3' Untranslated Regions, Adult, Aged, Case-Control Studies, Female, Gene Expression Regulation, Gene Frequency, Genetic Predisposition to Disease, genotype, Humans, Interleukin-12, Interleukin-12 Subunit p40, Leprosy, lepromatous, Male, Mexico, Middle Aged, Polymorphism, Genetic, RNA, Messenger}, author = {Alvarado-Navarro A and Montoya-Buelna M and Muñoz-Valle JF and Lopez-Roa RI and Guillen-Vargas C and Fafutis-Morris M}, title = {The 3'UTR 1188 A/C polymorphism in the interleukin-12p40 gene (IL-12B) is associated with lepromatous leprosy in the west of Mexico.}, abstract = {

Leprosy is a chronic infectious disease caused by Mycobacterium leprae. IL-12 participates in the immune response against M. leprae by regulating T cell differentiation into the Th1-type response. Several single nucleotide polymorphisms have been identified in the IL-12 gene such as 3'UTR 1188 A/C polymorphism, which is associated with different diseases. However, the relationship of this polymorphism with the immune response in leprosy has not been explored. In this case-control study, we evaluated 44 patients with lepromatous leprosy (LL) and 51 healthy subjects (HS). We aimed to determine the relationship between 3'UTR 1188 A/C polymorphism of IL-12 p40, mRNA expression, and soluble IL-12 concentration in LL patients and HS. Genotype frequencies were 41% A/A, 36% A/C, and 23% C/C in LL patients, and 47% A/A, 49% A/C, and 4% C/C in HS (p<0.05). LL patients had a lower mRNA expression of IL-12 p40 gene, whereas HS had a higher expression level. Soluble IL-12 p40 concentration was higher in LL patients than in HS (p<0.05). IL-12 p70 concentration did not differ between groups, and IL-12 p40 concentration was not significantly correlated with mRNA expression in either group. These data suggest that IL-12 p40 3'UTR 1188 A/C polymorphism is associated with greater susceptibility to lepromatous leprosy in patients from western Mexico, independently of IL-12 p40 and p70 expression levels.

}, year = {2008}, journal = {Immunology letters}, volume = {118}, pages = {148-51}, month = {2008 Jun 30}, issn = {0165-2478}, doi = {10.1016/j.imlet.2008.03.015}, language = {eng}, }