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Gene-selective transcription promotes the inhibition of tissue reparative macrophages by TNF

MPG-Autoren
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Dichtl,  Stefanie
Murray, Peter / Immunoregulation, Max Planck Institute of Biochemistry, Max Planck Society;

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Tanzer,  Maria C.
Mann, Matthias / Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Max Planck Society;

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Lindenthal,  Laura
Murray, Peter / Immunoregulation, Max Planck Institute of Biochemistry, Max Planck Society;

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Zeitler,  Leonie
Murray, Peter / Immunoregulation, Max Planck Institute of Biochemistry, Max Planck Society;

Strasser,  Alexander
Murray, Peter / Immunoregulation, Max Planck Institute of Biochemistry, Max Planck Society;

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Mann,  Matthias
Mann, Matthias / Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Max Planck Society;

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Murray,  Peter J.
Murray, Peter / Immunoregulation, Max Planck Institute of Biochemistry, Max Planck Society;

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Zitation

Dichtl, S., Sanin, D. E., Koss, C. K., Willenborg, S., Petzold, A., Tanzer, M. C., et al. (2022). Gene-selective transcription promotes the inhibition of tissue reparative macrophages by TNF. Life Science Alliance, 5(4): e202101315. doi:10.26508/lsa.202101315.


Zitierlink: https://hdl.handle.net/21.11116/0000-0009-EBF3-C
Zusammenfassung
Anti-TNF therapies are a core anti-inflammatory approach for chronic diseases such as rheumatoid arthritis and Crohn's Disease. Previously, we and others found that TNF blocks the emergence and function of alternative-activated or M2 macrophages involved in wound healing and tissue-reparative functions. Conceivably, anti-TNF drugs could mediate their protective effects in part by an altered balance of macrophage activity. To understand the mechanistic basis of how TNF regulates tissuetime-resolved phospho-proteomics, gene-specific approaches, metabolic analysis, and signaling pathway deconvolution. We found that TNF controls tissue-reparative macrophage gene expression in a highly gene-specific way, dependent on JNK signaling via the type 1 TNF receptor on specific populations of alternative-activated macrophages. We further determined that JNK signaling has a profound and broad effect on activated macrophage gene expression. Our findings suggest that TNF's anti-M2 effects evolved to specifically modulate components of tissue and reparative M2 macrophages and TNF is therefore a context-specific modulator of M2 macrophages rather than a pan M2 inhibitior.