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.