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BioMed Research International
Volume 2013, Article ID 459169, 7 pages
Clinical Study

Role of Toll-Interacting Protein Gene Polymorphisms in Leprosy Mexican Patients

1Centro Universitario de Tonalá, Universidad de Guadalajara, Tonalá, Jal., Mexico
2Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jal., Mexico
3CIINDE Universidad de Guadalajara/Instituto Dermatológico de Jalisco “Dr. Jose Barba Rubio”, Sierra Mojada 950, Edificio P. Primer Nivel, Colonia Independencia, 44340 Guadalajara, Jal., Mexico
4Genetic Division Department, Biomedical Research Center West, Instituto Mexicano del Seguro Social, Sierra Mojada 800, Colonia Independencia, 44340 Guadalajara, Jal., Mexico

Received 30 April 2013; Revised 9 September 2013; Accepted 14 September 2013

Academic Editor: Yoshio Ishibashi

Copyright © 2013 Margarita Montoya-Buelna et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Leprosy is a debilitating infectious disease of human skin and nerves. Genetics factors of the host play an important role in the disease susceptibility. Toll-interacting protein (TOLLIP) is an inhibitory adaptor protein within the toll-like receptor (TLR) pathway, which recognizes structurally conserved molecular patterns of microbial pathogens, initiating immune responses. The objective of this study was to investigate the association of variants in the TOLLIP gene with susceptibility to leprosy in Mexican patients. Methods. TOLLIP polymorphisms were studied using a case-control design of Mexican patients with lepromatous leprosy (LL). The polymorphisms of TOLLIP at loci −526 C>G (rs5743854), 1309956C>T (rs3750920), 1298430C>A (rs5744015), and 1292831 G>A (rs3750919) were analyzed by PCR, with sequence-specific primers in LL patients and healthy subjects (HS) as controls. Results. Genotype distributions were in Hardy Weinberg equilibrium for all sites except for rs3750920. Neither genotype nor allele frequencies were statistically different between LL patients and controls ( ). The maximum pairwise D’ coefficient reached was 0.44 of linkage ( ) for all the polymorphisms except for rs5743854. The three loci haplotype comparison yielded no significant differences between groups. Conclusions. Just the individuals with genotype C/C of rs3750920 have a trend of protective effect to developing LL.