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.