Considering the distinct roles of DC phenotypes and autophagy balance in Th differentiation, we propose a possible regulatory mechanisms: in T2 high asthma, DCs differentiate towards CD103+ DCs under long‐term allergen induction such as OVA, while in T2 low asthma, DCs are more likely to differentiate towards CD11b+ DCs under allergen and infection background. The gene discussed is ITGAE; the disease is infection.