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Updated: Feb 9, 2026

In Vitro Culture for H5N1-Specific Duck T Cells and Detection of Immune Responses Using Intracellular Cytokine Staining Method
Published on: May 30, 2025
Duck interferon regulatory factor 7 (IRF7) can control duck Tembusu virus (DTMUV) infection by triggering type I
Shun Chen1, Tao Wang2, Peng Liu2
1Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Chengdu, Sichuan 611130, China; Research Center of Avian Disease, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, Sichuan 611130, China; Key Laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Chengdu, Sichuan 611130, China.
Abstract:
Human interferon regulatory factor 7 (IRF7) plays an important role in the innate antiviral immune response. To date, the characteristics and functions of waterfowl IRF7 have not been clarified. This study reports the cDNA sequence, tissue distribution, and antiviral function of duck IRF7. The duck IRF7 gene has a 1536-bp open read frame (ORF) and encodes a 511-amino acid polypeptide. IRF7 is highly expressed in the blood and pancreas of 5-day-old ducklings and in the small intestine, large intestine and liver of 60-day-old adult ducks. Indirect immunofluorescence assay (IFA) showed that over-expressed duck IRF7 was located in both the cytoplasm and nucleus of transfected duck embryo fibroblasts (DEFs), which was also observed in poly(I:C)-stimulated or duck Tembusu virus (DTMUV)-infected DEFs. Titres and copies of DTMUV were significantly reduced in DEFs overexpressing IRF7. Moreover, overexpression of duck IRF7 significantly induced IFNα/β, but not IFNγ, mRNA expression, and transcription of downstream interferon-stimulated genes (ISGs), such as MX, OASL and IL-6, which were significantly induced by poly(I:C) co-stimulation, was enhanced. Additionally, duck IRF7 overexpression can significantly activate the IFNβ promoter in DEFs. Collectively, duck IRF7 plays an important role in host anti-DTMUV immune regulation, which depends on type I interferons and associated signal transduction pathway(s).
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