CSF3 enhances the innate immune responses to ALV-J infections via NF-κB and interferon pathways.

ABSTRACT: Avian leukosis viruses (ALVs) are a group of retroviruses with immunosuppressive and tumorigenic effects, causing substantial economic losses to the poultry industry due to the lack of effective commercial vaccines and antiviral drugs. Granulocyte colony-stimulating factor 3 (CSF3) is a cytokine that regulates hematopoiesis and modulates the proliferation and differentiation of immune cells. In our previous study, we unexpectedly observed that CSF3 expression was significantly upregulated upon stimulation with interferon-α (IFN-α) and ALV, suggesting a potential role in ALV infection. In this study, we confirmed that the CSF3 promoter could be activated by ALV and polyinosinic-polycytidylic acid (poly I:C) using a CSF3 promoter-driven reporter construct, and GAS potentially serving as the

SUBMITTER: Xia J 

PROVIDER: S-EPMC12362690 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature