Introduction
Allergic sensitization is the process of stimulating B cells and plasma cells with environmental antigens and releasing immunoglobulin E (IgE) antibodies in serum1. IgE is highly related to a variety of atopic diseases, such as asthma, atopic dermatitis, and rhinitis2,3.
The heritability of serum IgE levels ranges from 30% to 80% according to twin-based studies4,5, which underlies the importance of the genetic impact of IgE. Several genome-wide association studies (GWAS) demonstrated the correlation between genes and IgE6. The findings of significant regions varied between populations. Moffatt et al. demonstrated thatHLA-DR is significantly associated with IgE concentration in Caucasian ancestry7. A multi ancestry meta-analysis reveals that HLA-DQB1 *03:02 was reported as a genome-wide significant signal for IgE8 in Latino and Hispanic populations. More recently, the MHC region and IL4Rshowed significance with IgE in the Japanese population9. In contrast, no GWAS-significant signals of IgE were identified in a Han Chinese population-based study with a relatively small sample size10.
Earlier studies implicated the shared genetic components between IgE and atopic diseases8,11,12. The largest meta-analysis of the Caucasian population revealed that both HLA-DRB1 andIL4R/IL21R were related to IgE but had no association with asthma7. Kim et al. pointed out that there may be a genetic basis shared between IgE and atopic dermatitis13. However, the global genetic correlation and the local genetic correlation between these traits is still lacking.
Our study aimed to improve the understanding of the genetic architecture that affect IgE in a Taiwanese Han population and explore the pleiotropy effect between IgE and atopic diseases including asthma and atopic dermatitis. Finally, we constructed the PRS of IgE and explored the relationship between IgE PRS and allergic diseases.