1.1 Allergic rhinitis
AR is a disease with a high worldwide prevalence and is caused by common allergens encounterd in daily life, such as pollen, molds, and dust mites. AR causes symptoms such as sneezing, runny nose, nasal congestion, and itching, and also involves mucositis [5]. It is currently believed that pathogenic memory Th2 cells are important driving factors during the sensitization stage of AR [6]. Recent scRNA-seq studies of pathogenic cells and molecular mechanisms have revealed the complex heterogeneity cell types involved in AR. ScRNA-seq showed that monocytes are recruited to the nasal mucosa within hours of a local allergen attack, and macrophages carrying genes for Th2-related chemokines are highly expressed and have an activation phenotype driven by both IL-4 and IL-13 [7]. In addition to the increases in Th2 chemokines in ARstates, the levels of Th17 and Treg were also found to be significantly upregulated. The expression levels of Th17 related genes (S100A12 , PI3 , DEFB4A ) and histamine receptors (HRH1 and HRH2) were upregulated in the nasal mucosa of AR patients [8]. Su et al. [9] used scRNA-seq to conduct a clinical case-control study of 600 Chinese AR patients by extracting DNA from blood samples and found that polymorphisms in the TNFSF4 andBLK genes may be associated with susceptibility to AR in the Han Chinese population. Therefore, whether single cell sequencing can be used to further elucidate the complex gene environment interactions in AR will be the next challenge. Considering that AR has multiple clinical (phenotypic) and mechanistic (endotypic) forms, we can also look forward to current scRNA-seq methods providing better stratified therapeutic strategies based on detailed clinical and molecular diagnostics.