Related Experiment Video
Updated: Dec 18, 2025
Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein
Published on: April 21, 2015
Interferon-induced Transmembrane Protein 3 Prevents Acute Influenza Pathogenesis in Mice
1School of Public Health (Shenzhen), Sun Yat-sen University, Shenzhen 510275, Guangdong, China;National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Prevention and Control, Beijing 102206, China.
Objective:
Interferon-induced transmembrane protein 3 (IFITM3) is an important member of the IFITM family. However, the molecular mechanisms underlying its antiviral action have not been completely elucidated. Recent studies on IFITM3, particularly those focused on innate antiviral defense mechanisms, have shown that IFITM3 affects the body's adaptive immune response. The aim of this study was to determine the contribution of IFITM3 proteins to immune control of influenza infection in vivo.
Methods:
We performed proteomics, flow cytometry, and immunohistochemistry analysis and used bioinformatics tools to systematically compare and analyze the differences in natural killer (NK) cell numbers, their activation, and their immune function in the lungs of Ifitm3-/- and wild-type mice.
Results:
Ifitm3-/- mice developed more severe inflammation and apoptotic responses compared to wild-type mice. Moreover, the NK cell activation was higher in the lungs of Ifitm3-/- mice during acute influenza infection.
Conclusions:
Based on our results, we speculate that the NK cells are more readily activated in the absence of IFITM3, increasing mortality in Ifitm3-/- mice.
Insights
Interferon-induced transmembrane protein 3 (IFITM3) deficiency exacerbates influenza by increasing natural killer (NK) cell activation. Lack of IFITM3 leads to more severe inflammation and higher mortality in mice.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Interferon-induced transmembrane protein 3 (IFITM3) is crucial for innate antiviral defense.
- Its precise role in adaptive immunity and influenza control remains unclear.
- IFITM3 influences immune responses, but its in vivo contribution to influenza infection needs elucidation.
Purpose of the Study:
- To investigate the role of IFITM3 in the immune control of influenza infection in vivo.
- To determine IFITM3's contribution to the host's adaptive immune response against influenza.
Main Methods:
- Comparative analysis of Ifitm3-/- and wild-type mice.
- Proteomics, flow cytometry, and immunohistochemistry were employed.
- Bioinformatics tools were used to analyze NK cell numbers, activation, and function in lung tissues.
Main Results:
- Ifitm3-/- mice exhibited more severe inflammation and apoptosis.
- Elevated NK cell activation was observed in the lungs of Ifitm3-/- mice during acute influenza infection.
- These findings suggest a heightened innate immune response in the absence of IFITM3.
Conclusions:
- NK cell activation is increased in the absence of IFITM3.
- This enhanced NK cell activity may contribute to increased mortality in Ifitm3-/- mice during influenza infection.
- IFITM3 plays a protective role in modulating NK cell responses during viral infections.
