ArticleBMJ open2014
PARK2 and proinflammatory/anti-inflammatory cytokine gene interactions contribute to the susceptibility to leprosy: a case-control study of North Indian population.
Article in BMJ open, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 19 citations in OpenAlex.
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- The Microbiota and Evolution of Obesity.Endocrine reviews · 2025Review
- Family-based genetics identifies association of CUBN, IL1RL1 and PRKN variants with leprosy in Bangladesh.Scientific reports · 2025Article
- Leprosy: treatment, prevention, immune response and gene function.Frontiers in immunology · 2024Review
- Overexpression of Parkin in the Neuronal Progenitor Cells from a Patient with Parkinson's Disease Shifts the Transcriptome Towards the Normal State.Molecular neurobiology · 2023Article
- Distinct immune signatures discriminate between asymptomatic and presymptomatic SARS-CoV-2Cell research · 2021Article
- Transcriptomic Analysis ofFrontiers in cellular and infection microbiology · 2021Article
- Genetic Defects and Pro-inflammatory Cytokines in Parkinson's Disease.Frontiers in neurology · 2021Review
- Cell Biology of Intracellular Adaptation ofMicrobiology spectrum · 2019Review
- Article
- Identification of novel genetic loci GAL3ST4 and CHGB involved in susceptibility to leprosy.Scientific reports · 2017Article
- PINK1/Parkin-Dependent Mitochondrial Surveillance: From Pleiotropy to Parkinson's Disease.Frontiers in molecular neuroscience · 2017Review
- Common variants in the PARL and PINK1 genes increase the risk to leprosy in Han Chinese from South China.Scientific reports · 2016Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesCytokines and related molecules in immune-response pathways seem important in deciding the outcome of the host-pathogen interactions towards different polar forms in leprosy. We studied the role of significant and functionally important single-nucleotide polymorphisms (SNPs) in these genes, published independently from our research group, through combined interaction with an additional analysis of the in silico network outcome, to understand how these impact the susceptibility towards the disease, leprosy.
designThe study was designed to assess an overall combined contribution of significantly associated individual SNPs to reflect on epistatic interactions and their outcome in the form of the disease, leprosy. Furthermore, in silico approach was adopted to carry out protein-protein interaction study between PARK2 and proinflammatory/anti-inflammatory cytokines.
settingPopulation-based case-control study involved the data of North India. Protein-protein interaction networks were constructed using cytoscape.
participantsStudy included the data available from 2305 Northern Indians samples (829 patients with leprosy; 1476 healthy controls), generated by our research group. PRIMARY AND SECONDARY OUTCOME MEASURES: For genotype interaction analysis, all possible genotype combinations between selected SNPs were used as an independent variable, using binary logistic regression with the forward likelihood ratio method, keeping the gender as a covariate.
resultsInteraction analysis between PARK2 and significant SNPs of anti-inflammatory/proinflammatory cytokine genes, including BAT1 to BTNL2-DR spanning the HLA (6p21.3) region in a case-control comparison, showed that the combined analysis of: (1) PARK2, tumour necrosis factor (TNF), BTNL2-DR, interleukin (IL)-10, IL-6 and TGFBR2 increased the risk towards leprosy (OR=2.54); (2) PARK2, BAT1, NFKBIL1, LTA, TNF-LTB, IL12B and IL10RB provided increased protection (OR=0.26) in comparison with their individual contribution.
conclusionsEpistatic SNP-SNP interactions involving PARK2 and cytokine genes provide an additive risk towards leprosy susceptibility. Furthermore, in silico protein-protein interaction of PARK2 and important proinflammatory/anti-inflammatory molecules indicate that PARK2 is central to immune regulation, regulating the production of different cytokines on infection.
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