17q12-q21 variants interact with early-life exposures to modify asthma risk in Black children.
Jessica D GereigeAndreanne MorinAgustin CalatroniCynthia M VisnessRobert A WoodMeyer KattanLeonard B BacharierPatrice BeckerMatthew C AltmanJames E GernCarole OberGeorge T O'ConnorPublished in: Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology (2021)
Genetic factors and early-life exposures1 are both important determinants of childhood asthma. Among the more than 150 loci identified in genome-wide association studies (GWAS), 17q12-q21 is the most replicated childhood-onset asthma locus.2 Fine-mapping at this locus has been difficult in populations of European ancestry because of extensive linkage disequilibrium (LD) in this region. Taking advantage of the reduced LD in African ancestry populations, we3 and others4,5 have shown that single nucleotide polymorphisms (SNPs) in GSDMB are likely causal for childhood-onset asthma at this locus. However, it remains unclear whether the same variants underlie the many genotype-exposure interaction (GEI) effects.