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Your search keyword '"Berger, Wilhelm K."' showing total 7 results
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7 results on '"Berger, Wilhelm K."'

2. The retinoid X receptor has a critical role in synthetic rexinoid-induced increase in cellular all-trans-retinoic acid

Author

Belyaeva, Olga V., primary, Klyuyeva, Alla V., additional, Vyas, Ansh, additional, Berger, Wilhelm K., additional, Halasz, Laszlo, additional, Yu, Jianshi, additional, Atigadda, Venkatram R., additional, Slay, Aja, additional, Goggans, Kelli R., additional, Renfrow, Matthew B., additional, Kane, Maureen A., additional, Nagy, Laszlo, additional, and Kedishvili, Natalia Y., additional

Published
2024
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3. The epigenetic state of IL-4-polarized macrophages enables inflammatory cistromic expansion and extended synergistic response to TLR ligands

Author

Czimmerer, Zsolt, primary, Halasz, Laszlo, additional, Daniel, Bence, additional, Varga, Zsofia, additional, Bene, Krisztian, additional, Domokos, Apolka, additional, Hoeksema, Marten, additional, Shen, Zeyang, additional, Berger, Wilhelm K., additional, Cseh, Timea, additional, Jambrovics, Karoly, additional, Kolostyak, Zsuzsanna, additional, Fenyvesi, Ferenc, additional, Varadi, Judit, additional, Poliska, Szilard, additional, Hajas, Gyorgy, additional, Szatmari, Istvan, additional, Glass, Christopher K., additional, Bacsi, Attila, additional, and Nagy, Laszlo, additional

Published
2022
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4. A growth factor–expressing macrophage subpopulation orchestrates regenerative inflammation via GDF-15

Author

Patsalos, Andreas, primary, Halasz, Laszlo, additional, Medina-Serpas, Miguel A., additional, Berger, Wilhelm K., additional, Daniel, Bence, additional, Tzerpos, Petros, additional, Kiss, Máté, additional, Nagy, Gergely, additional, Fischer, Cornelius, additional, Simandi, Zoltan, additional, Varga, Tamas, additional, and Nagy, Laszlo, additional

Published
2021
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5. The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the late, stable epigenomic program of alternative macrophage polarization

Author

Daniel, Bence, primary, Czimmerer, Zsolt, additional, Halasz, Laszlo, additional, Boto, Pal, additional, Kolostyak, Zsuzsanna, additional, Poliska, Szilard, additional, Berger, Wilhelm K., additional, Tzerpos, Petros, additional, Nagy, Gergely, additional, Horvath, Attila, additional, Hajas, György, additional, Cseh, Timea, additional, Nagy, Aniko, additional, Sauer, Sascha, additional, Francois-Deleuze, Jean, additional, Szatmari, Istvan, additional, Bacsi, Attila, additional, and Nagy, Laszlo, additional

Published
2020
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6. A growth factor–expressing macrophage subpopulation orchestrates regenerative inflammation via GDF-15

Author

Patsalos, Andreas, Halasz, Laszlo, Medina-Serpas, Miguel A., Berger, Wilhelm K., Daniel, Bence, Tzerpos, Petros, Kiss, Máté, Nagy, Gergely, Fischer, Cornelius, Simandi, Zoltan, Varga, Tamas, and Nagy, Laszlo

Abstract

Muscle regeneration is the result of the concerted action of multiple cell types driven by the temporarily controlled phenotype switches of infiltrating monocyte–derived macrophages. Pro-inflammatory macrophages transition into a phenotype that drives tissue repair through the production of effectors such as growth factors. This orchestrated sequence of regenerative inflammatory events, which we termed regeneration-promoting program (RPP), is essential for proper repair. However, it is not well understood how specialized repair-macrophage identity develops in the RPP at the transcriptional level and how induced macrophage–derived factors coordinate tissue repair. Gene expression kinetics–based clustering of blood circulating Ly6Chigh, infiltrating inflammatory Ly6Chigh, and reparative Ly6Clow macrophages, isolated from injured muscle, identified the TGF-β superfamily member, GDF-15, as a component of the RPP. Myeloid GDF-15 is required for proper muscle regeneration following acute sterile injury, as revealed by gain- and loss-of-function studies. Mechanistically, GDF-15 acts both on proliferating myoblasts and on muscle-infiltrating myeloid cells. Epigenomic analyses of upstream regulators of Gdf15 expression identified that it is under the control of nuclear receptors RXR/PPARγ. Finally, immune single-cell RNA-seq profiling revealed that Gdf15 is coexpressed with other known muscle regeneration–associated growth factors, and their expression is limited to a unique subpopulation of repair-type macrophages (growth factor–expressing macrophages [GFEMs]).

Published
2022
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7. EGR2 is an epigenomic regulator of phagocytosis and antifungal immunity in alveolar macrophages.

Author

Kolostyak Z, Bojcsuk D, Baksa V, Szigeti ZM, Bene K, Czimmerer Z, Boto P, Fadel L, Poliska S, Halasz L, Tzerpos P, Berger WK, Villabona-Rueda A, Varga Z, Kovacs T, Patsalos A, Pap A, Vamosi G, Bai P, Dezso B, Spite M, D'Alessio FR, Szatmari I, and Nagy L

Subjects
Animals, Mice, Mice, Knockout, Mice, Inbred C57BL, Epigenomics, Epigenesis, Genetic immunology, Zymosan, Macrophages, Alveolar immunology, Macrophages, Alveolar metabolism, Early Growth Response Protein 2 genetics, Early Growth Response Protein 2 metabolism, Early Growth Response Protein 2 immunology, Phagocytosis immunology, Phagocytosis genetics, Aspergillus fumigatus immunology
Abstract

Alveolar macrophages (AMs) act as gatekeepers of the lung's immune responses, serving essential roles in recognizing and eliminating pathogens. The transcription factor (TF) early growth response 2 (EGR2) has been recently described as required for mature AMs in mice; however, its mechanisms of action have not been explored. Here, we identified EGR2 as an epigenomic regulator and likely direct proximal transcriptional activator in AMs using epigenomic approaches (RNA sequencing, ATAC sequencing, and CUT&RUN). The predicted direct proximal targets of EGR2 included a subset of AM identity genes and ones related to pathogen recognition, phagosome maturation, and adhesion, such as Clec7a, Atp6v0d2, Itgb2, Rhoc, and Tmsb10. We provided evidence that EGR2 deficiency led to impaired zymosan internalization and reduced the capacity to respond to Aspergillus fumigatus. Mechanistically, the lack of EGR2 altered the transcriptional response, secreted cytokines (i.e., CXCL11), and inflammation-resolving lipid mediators (i.e., RvE1) of AMs during in vivo zymosan-induced inflammation, which manifested in impaired resolution. Our findings demonstrated that EGR2 is a key proximal transcriptional activator and epigenomic bookmark in AMs responsible for select, distinct components of cell identity and a protective transcriptional and epigenomic program against fungi.

Published
2024
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