Abstract
Leprosy is an immunopathology caused by M. leprae; its evolution depends on immunological and genetic aspects of the host. The objective was verifying the relationship between SNPs 2029 and 2258 of the TLR-2 gene and leprosy. Blood samples from 127 individuals were analyzed: 45 patients, being 34 multibacillary (MB) and 11 paucibacillary (PB) and 82 contacts, in the municipalities of the State of Pará-Brazil. SNPs 2029 and 2258 of the TLR-2 gene were genotyped by sequencing on the ABI 3130 Genetic Analyzer (Applied Biosystems), analyzed using Fisher’s exact test. Distribution of SNP 2029 genotypes: all MB individuals presented the C/C genotype and the mutant (C/T) genotype was observed in contacts and PB. Alleles: all MB individuals presented only C allele and the mutant allele (T) was observed in contacts and PB. SNP 2258 genotypes: 79 contacts had G/G genotype and only 3 had G/A genotype, the MB group had only G/G genotype and the PB group was predominant G/G, with only 1 G/A genotype. Alleles: all MB individuals had allele G and the mutant allele (A) was observed in contacts and PB. The association between the SNPs and the susceptibility or protection to leprosy was not observed.
Highlights
Leprosy is an immunopathology caused by Mycobacterium leprae and the evolution of the infection depends on the host’s immunological and genetic factors, being the North region considered the area with the highest leprosy endemicity in Brazil [1] [2]
As for the distribution of the SNP 2029 genotypes of the toll like receptor 2 (TLR2) gene between the groups, it was observed that all MB individuals had the C/C genotype and the mutant genotype, C/T, was observed only in contacts and paucibacillaries
Several researches have been carried out in the field of molecular biology in order to ascertain the immunogenetic profile of the host against infections caused by mycobacteria, mainly due to the particularities regarding genes related to the cellular immune response Th1/Th2, in order to identify genetic components that may provide the opportunity for the infection to install in the host organism
Summary
Leprosy is an immunopathology caused by Mycobacterium leprae and the evolution of the infection depends on the host’s immunological and genetic factors, being the North region considered the area with the highest leprosy endemicity in Brazil [1] [2].Its tuberculoid (HT) (paucibacillary) form corresponds to high resistance to infection by M. leprae, being related to the Th1 cellular immune response. It is the form of high susceptibility, lepromatous leprosy (HV) (multibacillary), characterized by the deficiency of Th1 cellular immune response, excessive bacillary multiplication and spread of infection. Among these polar forms are the dimorphic forms of the disease. Several cells of the immune system are activated through their cell receptors to generate an antigenic response, such as Natural Killer cells, lymphocytes, among others. Among the receptors expressed by Natural Killer cells, the Toll-Like receptors (TLR) on the surface and cellular cytoplasm stand out in the innate immune response [6] [7]
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