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The present study aimed to explore the microRNA‑let‑7e (miR‑let‑7e) expression in allergic rhinitis (AR), and to investigate the underlying molecular mechanisms. miR‑let‑7e expression in the nasal mucosa of mice and patients with AR were detected. The expression levels of three inflammatory factors, including histamine, immunoglobulin E and tumor necrosis factor‑α (TNF‑α), in the blood of AR mice and in interleukin (IL)‑13‑stimulated nasal epithelial cells (NECs) were also measured. Furthermore, the target gene of miR‑let‑7e was predicted and validated using a luciferase reporter assay. The expression levels of Janus kinase 1 (JAK1) and signal transducer and activator of transcription 3 (STAT3) were detected. The results demonstrated that miR‑let‑7e was downregulated in patients and mice with AR compared with the controls. In addition, the expression levels of inflammatory factors were higher in the blood of mice with AR compared with the control group, while miR‑let‑7e overexpression inhibited these levels in AR mice and IL‑13‑stimulated NECs. Furthermore, suppressor of cytokine signaling 4 (SOCS4) was revealed as a potential target gene of miR‑let‑7e and was negatively regulated by miR‑let‑7e. Overexpression of SOCS4 abrogated the anti‑inflammatory activity of miR‑let‑7e overexpression. Finally, miR‑let‑7e overexpression activated the JAK1/STAT3 signaling pathway. In conclusion, miR‑let‑7e may serve an important role in the progression and development of AR, while overexpression of miR‑let‑7e had an anti‑inflammatory effect by targeting SOCS4, which may be achieved by activation of the JAK1/STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]