The current view is that allergic rhinitis is a polygenic disease, controlled by a combination of genetic and environmental factors, with heritabilities ranging from 0.33 to 0.75, as well as gene-gene and gene-environment interactions. In genetically susceptible hosts, the development of atopy to a particular allergen requires appropriate exposure and subsequent accumulation of specific IgE antibody responses. The development of allergic rhinitis is the result of chronic low-dose exposure to major allergens, such as indoor environments.
Because multiple allergic disease phenotypes, such as asthma, allergic rhinitis, and atopic dermatitis, share many of the same systemic features, such as total serum IgE and specific IgE, and because multiple clinical phenotypes often occur together, Barnes et al. have proposed that “allergic diseases may share a common genetic basis” and have provided an explanation for their genetics. Barnes et al. proposed that “allergic diseases may share a common genetic basis” and proposed a hypothesis for the genetic pattern: that there may be some genes specific for various clinical phenotypes of allergic diseases and some genes common to allergic diseases. According to this hypothesis, the genes controlling the expression of allergic diseases can be divided into at least three categories: the first is the immune-responsive genes, which control the specific immune response, the latter being initiated to some extent by environmental stimuli; the second is the non-specific genes, which determine the general propensity to synthesize various specific IgE; and the third is the clinical phenotype-specific genes.
Regarding the genetic pattern of allergic diseases, Barnes et al. also provided us with a possible model (see Figure 1) where there may be a set of “immune-mediated disease genes” that are essential for the primary and/or secondary regulation of immune system diseases; it is assumed that different groups of genes are associated with different types of Barnes et al. also predicted several specific clusters of major genes, which are included in each of the different clinical traits or manifestations of the above phenotypes (e.g., overall upregulation of IgE and/or inflammatory response); another group of genes has a major impact on respiratory inflammation and hyperresponsiveness, which can easily be associated with respiratory-specific genes and/or certain combinations of genes associated with severity, largely based on the idea that “asthma and allergic rhinitis are one airway, one disease. Barnes suggests that there may be a common gene associated with both asthma and AR, and that additional genes (e.g., modifier genes) determine the ultimate risk of developing asthma. Finally, environmental influences are also major determinants of the complex chimera of allergic disease phenotypes. Environmental exposure factors and genotype together determine the final disease, and individual body composition has an influence on the risk of developing the disease. Environmental factors can be divided into two categories, namely, specific environmental factors that directly involve allergens in allergic reactions and non-specific environmental factors that induce or aggravate the symptoms of allergic reactions.