Mouse IFN-Alpha 4 is a widely expressed mouse IFN-Alpha which may play a role in preparing cells to express high levels of other mouse interferon alpha subtypes upon viral infection.

• Exhibits higher antiviral potency than Mouse IFN-Alpha A in standard CPE assay
• Authentic sequence provides a better model of native Mouse IFN-Alpha 4
• Member of Mouse Type I IFN with early endogenous expression

Background

Mouse IFN-Alpha 4 was initially cloned by Zwarthoff et al. [(1985) Nuc. Acids Res. 13(3)791], and has been extensively studied. It is apparently expressed early in viral infection in a protein synthesis independent manner, and its expression is induced by phosphorylation of IRF-3. It may be that Mouse IFN-Alpha 4, like IFN Beta, has a priming function on cells, enabling the expression of other Mouse IFN-Alpha subtypes [Review by Mesplede et al., (2003) Autoimmunity 36(8):447 and Asselin-Paturel & Trinchieri (2005) J. Exp. Med. 202(4):461]. Thus, this interferon is among the first observed after viral infection. Intriguingly, while this interferon is expressed in a large variety of cell types, one report suggests that the expression level in dendritic cells is low to non-existent [Barchet et al., (2002) J. Exp. Med. 195(4):507].

Summary: Mouse IFN-Alpha 4 is a widely expressed mouse IFN-Alpha which may play a role in preparing cells to express high levels of other mouse interferon alpha subtypes upon viral infection.

For more information on Mouse IFN-Alpha subtype nomenclature click here.

8 Citations

1. Li, N. et al., (2023), "STING controls opioidinduced itch and chronic itch via spinal tank-binding kinase 1-dependent type I interferon response in mice", J. Neuroinflammation, 20(1):101, PMID: 37122031, DOI: 10.1186/s12974-023-02783-0 (link)


2. Lee, J.V. et al., (2022), Combinatorial immunotherapeuties overcome MYC-driven immune evasion in triple negative breast cancer, Nat. Commun., 13(1):3671, PMID: 35760778, DOI: 10.1038/s41467-022-31238-y (link)


3. Throm, Allison, et al. (2018). Dysregulated NK Cell PLC-gamma-2 Signaling and Activity in Juvenile Dermatomyositis. JCI Insight, 14 pgs. PMID: 30429375. (link)


4. Wang, Kuan-Chung (2018). Dichotomy of TNF Family Ligands Expression on Classical Dendritic Cells and Monocyte-Derived Antigen Presenting Cells During Viral Infection. University of Toronto, 92 pgs. PMID: no PMID. (link)


5. Kalkavan, Halime, et al. (2017). Spatiotemporally Restricted Arenavirus Replication Induces Immune Surveillance and Type I Interferon-Dependent Tumour Regression. Nature Communications, 14 pgs. PMID: 28248314. (link)


6. Shaabani, Namir, et al. (2016). CD169+ Macrophages Regulate PD-L1 Expression via Type I Interferon and Thereby Prevent Severe Immunopathology After LCMV Infection. Cell Death Differentiation Association, 10 pgs. PMID: 27809306. (link)


7. Hu, MM, et al. (2015). TRIM38 Negatively Regulates TLR3/4-Mediated Innate Immune and Inflammatory Responses by Two Sequential and Distinct Mechanisms. Journal of Immunology, 12 pgs. PMID: 26392463. (link)


8. Levy, David (2002). Whence Interferon? Variety in the Production of Interferon in Response to Viral Infection. JEM, 4 pgs. PMID: 11854366. (link)

References

1. Van Pesch et al. 2004.


2. Zwarthoff et al. (1985) Nuc. Acids Res. 13(3) 791.


3. Mesplede et al. (2003) Autoimmunity 36(8):447.


4. Asselin-Paturel & Trinchieri (2005) J. Exp. Med. 202(4):461.


5. Barchet et al. (2002) J. Exp. Med. 195(4):507.