The TLR1 gene is associated with higher protection from leprosy in women

PLoS One. 2018 Oct 5;13(10):e0205234. doi: 10.1371/journal.pone.0205234. eCollection 2018.

Abstract

Leprosy is an infectious disease with a complex genetic and immunological background. Polymorphisms in genes that encode cytokines and receptors involved in the immune response, such as the Toll-like receptor 1 (TLR1), may be associated with disease risk. We hypothesized that polymorphisms in innate immunity genes confer susceptibility to leprosy that differs between women and men. In this study, we investigate sex differences in the association between a single nucleotide polymorphism (SNP) in TLR1 and Nucleotide-binding oligomerization domain containing 2 (NOD2) genes and leprosy susceptibility in 256 clinically classified leprosy patients and 233 control subjects in a Brazilian population. Our results showed no association between the SNP rs8057341 in NOD2 and leprosy in this population. However, the heterozygous genotype of the TLR1 SNP (rs4833095) showed a statistically significant association in women (OR = 0.54, P = 0.02). Our findings suggest that the TLR1 polymorphism was associated with an increased protection from leprosy in women.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Biopsy
  • Brazil
  • Case-Control Studies
  • Female
  • Genetic Predisposition to Disease*
  • Genotype
  • Humans
  • Immunity, Innate / genetics*
  • Leprosy / genetics*
  • Leprosy / immunology
  • Leprosy / pathology
  • Male
  • Middle Aged
  • Nod2 Signaling Adaptor Protein / genetics*
  • Polymorphism, Single Nucleotide
  • Sequence Analysis, DNA
  • Sex Factors
  • Skin / pathology
  • Toll-Like Receptor 1 / genetics*
  • Toll-Like Receptor 1 / immunology

Substances

  • NOD2 protein, human
  • Nod2 Signaling Adaptor Protein
  • TLR1 protein, human
  • Toll-Like Receptor 1

Grants and funding

This study was funded by Health Surveillance Secretariat of the Ministry of Health. Government of Brazil (Grant number: 23072.039742 / 2012-29) to FCFL. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.