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[Show abstract][Hide abstract] ABSTRACT: Leprosy is the major cause of non-traumatic neuropathy. Herein, we investigated the role of ninjurin 1, an adhesion molecule involved in nerve regeneration in leprosy. Our results demonstrated that M. leprae stimulates in vitro up-regulation of ninjurin mRNA in cultured Schwann and blood cells as well as in vivo mRNA and protein expression in leprosy nerve biopsies. A polymorphism (asp110ala) was investigated in a case-control study (1123 individuals) and no association was found with leprosy per se or with disseminated forms. Nevertheless, ala110 was associated with functional nerve impairment (OR=2.42; p=0.02 for ala/ala) and with lower mRNA levels. Our data suggests that asp110ala could be a valuable genetic marker of nerve damage in leprosy.
Journal of Neuroimmunology 11/2007; 190(1-2):131-8. DOI:10.1016/j.jneuroim.2007.07.015 · 2.79 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Many genes including HLA, KIR, and MICA genes, as well as polymorphisms in cytokines have been investigated for their role in infectious disease. HLA alleles may influence not only susceptibility or resistance to leprosy, but also the course of the disease. Some combinations of HLA and KIR may result in negative as well as positive interactions between NK cells and infected host cells with M. leprae, resulting in activation or inhibition of NK cells and, consequently, in death of bacillus. In addition, studies have demonstrated the influence of MICA genes in the pathogenesis of leprosy. Specifically, they may play a role in the interaction between NK cells and infected cells. Finally, pro- and anti-inflammatory cytokines have been influencing the clinical course of leprosy. Data from a wide variety of sources support the existence of genetic factors influencing the leprosy pathogenesis. These sources include twin studies, segregation analyses, family-based linkage and association studies, candidate gene association studies, and, most recently, genome-wide association studies (GWAS). The purpose of this brief review was to highlight the importance of some immune response genes and their correlation with the clinical forms of leprosy, as well as their implications for disease resistance and susceptibility.
[Show abstract][Hide abstract] ABSTRACT: Several host and environmental factors contribute to tuberculosis outcome, interestingly single nucleotide polymorphisms (SNPs) in candidate genes have been evaluated in populations with different ethnicities and TB infection. In the present study we focused on SNPs in cytokine and inflammatory mediator genes: tumor necrosis factor (TNF) -308G>A (rs1800629), interleukin-10 (IL10) -819C>T (rs1800871), interferon-gamma (IFNG) +874T>A (rs2430561), and leukotriene A4 hydrolase (LTA4H) rs1978331, rs17525495 and rs2660898 in a case-control study involving 102 pulmonary tuberculosis patients and 456 controls from Mozambique. LTA4H, IL10 and IFNG SNPs showed no associations with pulmonary tuberculosis. However, distribution of the TNF -308A allele, genotype and carrier frequencies showed a significant risk association with tuberculosis that was maintained after adjustment for non-genetic variables and Bonferroni correction (AA genotype, OR = 1.9, p Bonf < 0.001; A allele OR = 2.9, p Bonf = 0.005 and GA/AA carrier OR = 2.6, p Bonf = 0.035). Interestingly, this association has not been reported in a sub-Saharan African population before. Our results suggest a role of -308 TNF polymorphism and tuberculosis susceptibility.