Measles contributes to rheumatoid arthritis: evidence from pathway and network analyses of genome-wide association studies

PLoS One. 2013 Oct 18;8(10):e75951. doi: 10.1371/journal.pone.0075951. eCollection 2013.

Abstract

Growing evidence from epidemiological studies indicates the association between rheumatoid arthritis (RA) and measles. However, the exact mechanism for this association is still unclear now. We consider that the strong association between both diseases may be caused by shared genetic pathways. We performed a pathway analysis of large-scale RA genome-wide association studies (GWAS) dataset with 5,539 cases and 20,169 controls of European descent. Meanwhile, we evaluated our findings using previously identified RA loci, protein-protein interaction network and previous results from pathway analysis of RA and other autoimmune diseases GWAS. We confirmed four pathways including Cytokine-cytokine receptor interaction, Jak-STAT signaling, T cell receptor signaling and Cell adhesion molecules. Meanwhile, we highlighted for the first time the involvement of Measles and Intestinal immune network for IgA production pathways in RA. Our results may explain the strong association between RA and measles, which may be caused by the shared genetic pathway. We believe that our results will be helpful for future genetic studies in RA pathogenesis and may significantly assist in the development of therapeutic strategies.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Arthritis, Rheumatoid / complications*
  • Arthritis, Rheumatoid / genetics*
  • Arthritis, Rheumatoid / metabolism
  • Autoimmune Diseases / genetics
  • Autoimmune Diseases / metabolism
  • Gene Regulatory Networks
  • Genetic Predisposition to Disease
  • Genome-Wide Association Study*
  • Humans
  • Measles / complications*
  • Measles / genetics*
  • Measles / metabolism
  • Protein Interaction Maps
  • Reproducibility of Results
  • Signal Transduction

Grants and funding

This work was supported by funding from the National Nature Science Foundation of China (grant numbers 81300945, 31200934, 31171219, 81271213, 81070878, 81271214, and 81261120404), the Natural Science Foundation of Guangdong Province, China (No S2012010008222), and the Science and Technology Innovation Fund of Guangdong Medical College (No. STIF 201101). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.