Genetic Architecture of Adaptive Immune System Identifies Key Immune Regulators

Cell Rep. 2018 Oct 16;25(3):798-810.e6. doi: 10.1016/j.celrep.2018.09.048.

Abstract

The immune system is highly diverse, but characterization of its genetic architecture has lagged behind the vast progress made by genome-wide association studies (GWASs) of emergent diseases. Our GWAS for 54 functionally relevant phenotypes of the adaptive immune system in 489 healthy individuals identifies eight genome-wide significant associations explaining 6%-20% of variance. Coding and splicing variants in PTPRC and COMMD10 are involved in memory T cell differentiation. Genetic variation controlling disease-relevant T helper cell subsets includes RICTOR and STON2 associated with Th2 and Th17, respectively, and the interferon-lambda locus controlling regulatory T cell proliferation. Early and memory B cell differentiation stages are associated with variation in LARP1B and SP4. Finally, the latrophilin family member ADGRL2 correlates with baseline pro-inflammatory interleukin-6 levels. Suggestive associations reveal mechanisms of autoimmune disease associations, in particular related to pro-inflammatory cytokine production. Pinpointing these key human immune regulators offers attractive therapeutic perspectives.

Keywords: adaptive immune system; association; autoimmunity; genetics; genome-wide association; immune phenotype; susceptibility.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Autoimmune Diseases / genetics*
  • Autoimmune Diseases / immunology
  • Autoimmune Diseases / pathology
  • Female
  • Gene Expression Profiling
  • Gene Expression Regulation*
  • Genetic Predisposition to Disease*
  • Genome-Wide Association Study*
  • Healthy Volunteers
  • Humans
  • Immunologic Factors / genetics*
  • Male
  • Middle Aged
  • Polymorphism, Single Nucleotide*
  • T-Lymphocytes, Regulatory / immunology
  • T-Lymphocytes, Regulatory / metabolism
  • Th17 Cells / immunology
  • Th17 Cells / metabolism
  • Young Adult

Substances

  • Immunologic Factors