Dichtl, Stefanie ORCID: 0000-0002-7657-329X, Sanin, David E., Koss, Carolin K., Willenborg, Sebastian, Petzold, Andreas, Tanzer, Maria C., Dahl, Andreas ORCID: 0000-0002-2668-8371, Kabat, Agnieszka M., Lindenthal, Laura, Zeitler, Leonie ORCID: 0000-0002-9090-0795, Satzinger, Sabrina ORCID: 0000-0001-8173-8696, Strasser, Alexander, Mann, Matthias, Roers, Axel, Eming, Sabine A., El Kasmi, Karim C., Pearce, Edward J. and Murray, Peter J. (2022). Gene-selective transcription promotes the inhibition of tissue reparative macrophages by TNF. Life Sci. Alliance, 5 (4). COLD SPRING HARBOR: LIFE SCIENCE ALLIANCE LLC. ISSN 2575-1077

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Abstract

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.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Dichtl, StefanieUNSPECIFIEDorcid.org/0000-0002-7657-329XUNSPECIFIED
Sanin, David E.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Koss, Carolin K.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Willenborg, SebastianUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Petzold, AndreasUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Tanzer, Maria C.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Dahl, AndreasUNSPECIFIEDorcid.org/0000-0002-2668-8371UNSPECIFIED
Kabat, Agnieszka M.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Lindenthal, LauraUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Zeitler, LeonieUNSPECIFIEDorcid.org/0000-0002-9090-0795UNSPECIFIED
Satzinger, SabrinaUNSPECIFIEDorcid.org/0000-0001-8173-8696UNSPECIFIED
Strasser, AlexanderUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Mann, MatthiasUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Roers, AxelUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Eming, Sabine A.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
El Kasmi, Karim C.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Pearce, Edward J.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Murray, Peter J.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-685753
DOI: 10.26508/lsa.202101315
Journal or Publication Title: Life Sci. Alliance
Volume: 5
Number: 4
Date: 2022
Publisher: LIFE SCIENCE ALLIANCE LLC
Place of Publication: COLD SPRING HARBOR
ISSN: 2575-1077
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
C-JUN; ALTERNATIVE ACTIVATION; MOUSE DEVELOPMENT; MESSENGER-RNA; IN-VIVO; EXPRESSION; AP-1; JNK; APOPTOSIS; IDENTIFICATIONMultiple languages
BiologyMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/68575

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