ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
MAPKAP kinase 3 suppresses Ifng gene expression and attenuates NK cell cytotoxicity and Th1 CD4 T-cell development upon influenza A virus infection.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Replication-incompetent influenza A viruses armed with IFN-γ effectively mediate immune modulation and tumor destruction in mice harboring lung cancer.Molecular therapy oncolytics · 2023Article
- A novel lncRNA DFRV plays a dual function in influenza A virus infection.Frontiers in microbiology · 2023Article
- The Two Sides of the Same Coin-Influenza Virus and Intracellular Signal Transduction.Cold Spring Harbor perspectives in medicine · 2021Review
- Stimulus-Specific Expression, Selective Generation and Novel Function of Grass Carp (Frontiers in immunology · 2021Article
- MAPK Activated Protein Kinase 3 Is a Prognostic-Related Biomarker and Associated With Immune Infiltrates in Glioma.Frontiers in oncology · 2021Article
- PD-1 IC Inhibition Synergistically Improves Influenza A Virus-Mediated Oncolysis of Metastatic Pulmonary Melanoma.Molecular therapy oncolytics · 2020Article
- Article
- Pharmacological and genetic inhibition of downstream targets of p38 MAPK in experimental nephrotic syndrome.American journal of physiology. Renal physiology · 2018Article
- Oncolytic influenza virus infection restores immunocompetence of lung tumor-associated alveolar macrophages.OncoimmunologyArticle
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
MK2 and MK3 are downstream targets of p38 and ERK1/2. They control the mRNA stability of several inflammatory cytokines, including TNF-α and IL-10. Whereas MK2 is expressed ubiquitously, the expression of MK3 is restricted to muscle, liver, and heart tissues and T and NK cells. Using Mk-deficient and wild-type (WT) mice, we demonstrated an inhibitory effect of MK3, but not of MK2, on interferon (IFN)-γ expression in T and NK lymphocytes. The results provided evidence that the inhibitory effect of MK3 is based on negative feedback phosphorylation of p38 and ERK1/2, which causes decreased binding of Stat4 to the IFN-γ promoter and reduced expression of IFN-γ mRNA and protein. Consequently, all Mk3(-/-) mice challenged with the Th1-inducing influenza A virus (IAV) survived the WT LD50 virus dose. The reduced disease severity in the Mk3(-/-) mice was accompanied by a >10-fold reduction in viral lung titer and an increase in the number of activated NK cells and enhanced Th1 activation of CD4 T cells. Thus, our data describe the protein kinase MK3 as a novel regulator of the innate and adaptive immune responses.-Köther, K., Nordhoff, C., Masemann, D., Varga, G., Bream, J. H., Gaestel, M., Wixler, V., Ludwig, S. MAPKAP kinase 3 suppresses Ifng gene expression and attenuates NK cell cytotoxicity and Th1 CD4 T-cell development upon influenza A virus infection.
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