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NMP4: a nuclear driver of innate inflammatory responses during influenza A virus infection

Cellular & Molecular Immunology volume 17, pages 1220–1221 (2020)Cite this article

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Infection with influenza A virus (IAV) results in an acute respiratory disease with a highly variable pathogenesis. Viral infection triggers various inflammatory mechanisms that promote viral clearance on the one hand but can have deleterious effects on pulmonary tissue integrity on the other hand. A detailed knowledge of the mechanisms involved in the antiviral immune responses to IAV is key for a better understanding the concept of host susceptibility and eventually for the design of future therapeutic treatment strategies. In their latest publication in Mucosal Immunology, Yang et al. highlight a pivotal role of the transcription factor nuclear matrix protein 4 (NMP4) in driving inflammatory recruitment of monocytes and neutrophils and increasing disease severity during IAV infection.1

The transcription factor NMP4 was previously shown to promote Il1b transcription and the development of arthritis,9 indicating its role in driving immunopathology, but the implications of Nmp4-mediated signaling for host defense and immune regulation during infection are unknown.

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Authors and Affiliations

  1. Infection Immunology Group, Institute of Medical Microbiology, Infection Control and Prevention, Health Campus Immunology, Infectiology and Inflammation, Otto-von-Guericke University, Magdeburg, Germany

    Julia D. Boehme, Sarah Frentzel & Dunja Bruder

  2. Immune Regulation Group, Helmholtz Centre for Infection Research, Braunschweig, Germany

    Julia D. Boehme, Sarah Frentzel & Dunja Bruder

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  1. Julia D. Boehme
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  2. Sarah Frentzel
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  3. Dunja Bruder
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Correspondence to Dunja Bruder.

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The authors declare no competing interests.

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Boehme, J.D., Frentzel, S. & Bruder, D. NMP4: a nuclear driver of innate inflammatory responses during influenza A virus infection. Cell Mol Immunol 17, 1220–1221 (2020). https://doi.org/10.1038/s41423-020-0517-5

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  • DOI: https://doi.org/10.1038/s41423-020-0517-5

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