Lack of association of (rs1800896) and (rs1800925) with non-segmental vitiligo susceptibility in South Indian population.

Kalai Selvi Rajendiran, Medha Rajappa, Laxmisha Chandrashekar, D M Thappa, Panneer Devaraju
Author Information
  1. Kalai Selvi Rajendiran: Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India.
  2. Medha Rajappa: Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India.
  3. Laxmisha Chandrashekar: Department of Dermatology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India.
  4. D M Thappa: Department of Dermatology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India.
  5. Panneer Devaraju: Unit of Microbiology and Molecular Biology, Indian Council of Medical Research-Vector Control Research Centre, Puducherry, India.

Abstract

BACKGROUND: Vitiligo is an autoimmune depigmentation disorder caused by multiple etiologies. Genetic polymorphisms in cytokine genes influence their expression and augment disease development. Analyzing the influence of genetic polymorphisms will help in better understanding of the complex etiopathogenesis of vitiligo.
AIM: To study the influence of interleukin IL-10 (rs1800896) and IL-13 (rs1800925) polymorphisms on vitiligo risk in South Indian population.
METHODS: Two hundred and sixty-four vitiligo patients and 264 controls were recruited in this study. Genotyping was done by quantitative PCR and plasma cytokine levels were measured by ELISA.
RESULTS: Allele frequencies of IL-10 (rs1800896) and IL-13 (rs1800925) SNPs were observed to be equal in the groups. Mutant allele G of IL-10 (rs1800896) enhanced the familial inheritance of vitiligo (P < 0.0001, OR-25.1, 95% CI-7.64-82.7) and influenced the development of vulgaris type of vitiligo (P = 0.034, OR-1.83, 95% CI-1.07-3.13). Ancestral allele A of IL-10 (rs1800896) conferred protection against development of acrofacial vitiligo (P = 0.04, OR-0.56, 95% CI-0.33-0.95). Circulatory IL-10 levels in vitiligo patients were higher than controls (P < 0.0001). Individuals with genotype GG of IL-10 (rs1800896) had the highest circulatory levels of IL-10 (P < 0.0001). Among the genotypes of IL-13 (rs1800925) variant, none influenced the phenotype of nonsegmental vitiligo such as gender, family history, age of onset and types of vitiligo (P > 0.05). In addition, no difference was noted in the circulatory levels of IL-13 between patients and controls (P = 0.48). Within patients, CC genotype of IL-13 (rs1800925) was observed to enhance the circulatory IL-13 levels (P < 0.0001).
LIMITATION: Replication group analysis in a larger multicentric cohort in future would validate further understanding of vitiligo susceptibility in South Indian ethnics.
CONCLUSION: IL-10 (rs1800896) and IL-13 (rs1800925) polymorphisms did not confer risk to develop vitiligo in South Indian population.

Keywords

MeSH Term

Adult
Biomarkers
Disease Susceptibility
Female
Genetic Association Studies
Genetic Predisposition to Disease
Humans
India
Interleukin-10
Interleukin-13
Male
Middle Aged
Polymorphism, Single Nucleotide
Population Surveillance
Vitiligo

Chemicals

Biomarkers
IL10 protein, human
Interleukin-13
Interleukin-10

Word Cloud

Created with Highcharts 10.0.0vitiligoIL-10rs1800896P0IL-13rs1800925polymorphismslevelsSouthIndianpatients<0001influencedevelopmentpopulationcontrols95%=circulatoryGeneticcytokineunderstandingstudyriskobservedalleleinfluencedgenotypesusceptibilityBACKGROUND:VitiligoautoimmunedepigmentationdisordercausedmultipleetiologiesgenesexpressionaugmentdiseaseAnalyzinggeneticwillhelpbettercomplexetiopathogenesisAIM:interleukinMETHODS:Twohundredsixty-four264recruitedGenotypingdonequantitativePCRplasmameasuredELISARESULTS:AllelefrequenciesSNPsequalgroupsMutantGenhancedfamilialinheritanceOR-251CI-764-827vulgaristype034OR-183CI-107-313Ancestralconferredprotectionacrofacial04OR-056CI-033-095CirculatoryhigherIndividualsGGhighestAmonggenotypesvariantnonephenotypenonsegmentalgenderfamilyhistoryageonsettypes>05additiondifferencenoted48WithinCCenhanceLIMITATION:ReplicationgroupanalysislargermulticentriccohortfuturevalidateethnicsCONCLUSION:conferdevelopLackassociationnon-segmentalinterleukins

Similar Articles

Cited By