The above interaction and pathway analysis allows us to propose that the complex genetic background is the predominant factor for the outcome of the disease, where the combined effect of the variant risk alleles of the PARK2 gene, responsible for affecting transcription binding site and lowering the expression of the reporter gene by in vitro experiment, 18 along with the risk alleles of the anti-inflammatory cytokine genes—IL-10, IL-6, TGFBR2, responsible for lowering the CMI response towards the invading bacteria and proinflammatory cytokines—TNFα, is responsible in providing highly significant risk towards leprosy.
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PARK2 and proinflammatory/anti-inflammatory cytokine gene interactions contribute to the susceptibility to leprosy: a case-control study of North Indian population.
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