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Articles by Manfred Kopf
RNA-LNP–mediated in vivo prime editing corrects disease phenotypes in a mouse model of citrullinemia type I
Editor’s summary Abstract Supplementary Materials REFERENCES AND NOTES Information & Authors Metrics & Citations Check Access References Figures Tables Media Share Editor’s summary Urea cycle disorders include citrullinemia type I (CTLN1), which is caused by pathogenic variants in the argininosuccinate synthetase 1 (ASS1) gene.
A Lymphotoxin-Driven Pathway to Hepatocellular Carcinoma
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Main text (Cancer Cell 16, 295–308; October 6, 2009) We, the authors of this publication, described the role of lymphotoxin signaling in the development of hepatocellular carcinoma. We have become aware of several errors involving duplicated images in the figures. Specifically, in Figure 7E (group tg1223 Tnfr1−/−), three consecutive liver sections stained for H&E, B220, and CD3 were duplicated in Figure S7B (group tg1223IKKβF/F).
By Johannes Haybaeck, Monika Wolf, Achim Weber, Ulrich Wagner, Michael Kurrer, Juliane Bremer, Pierre-Alain Clavien, Robert Thimme, Hubert Erich Blum, Sergei A. Nedospasov, Kurt Zatloukal, Muhammad Ramzan, Sandra Ciesek, Thomas Pietschmann, Patrice N. Marche, Michael Karin, Manfred Kopf, Jeffrey L. Browning, Adriano Aguzzi, Mathias Heikenwalder, Nicolas Zeller, Giandomenica Iezzi
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Cell Press
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Peroxisomes are critical for a unique metabolic demand and survival of alveolar macrophages
Keywords innate immunity tissue-resident macrophages immunometabolism peroxisomes Research topic(s) CP: Immunology CP: Metabolism Introduction Tissue-resident macrophages (TRMs) are part of the innate immune system that act as immune sentinels to maintain tissue homeostasis and provide defense against pathogen invasion.1 They are strategically distributed among various tissues and are readily capable of metabolic adaptation to microenvironmental factors, such as limited fuel sources,...
The thioredoxin system: balancing redox responses in immune cells and tumors
Abstract The thioredoxin (TRX) system is an important contributor to cellular redox balance and regulates cell growth, apoptosis, gene expression, and antioxidant defense in nearly all living cells. Oxidative stress, the imbalance between reactive oxygen species (ROS) and antioxidants, can lead cell death and tissue damage, thereby contributing to ageing and to the development of several diseases, including cardiovascular and allergic diseases, diabetes, and neurological disorders.
Comparative analysis of the role of mast cells in murine asthma models using Kit‐sufficient mast cell‐deficient animals
ORIGINAL ARTICLE Manfred Kopf Corresponding Author manfred.kopf@biol.ethz.ch Institute of Molecular Health Sciences, ETH Zurich, Zurich, Switzerland Correspondence Luigi Tortola, Institute for Molecular Health Sciences, Department of Biology, ETH Zurich, Otto‐Stern Weg 7, 8093 Zurich, Switzerland. Email: luigi.tortola@biol.ethz.ch Manfred Kopf, Institute for Molecular Health Sciences, Department of Biology, ETH Zurich, Otto‐Stern Weg 7, 8093 Zurich, Switzerland.
Redox regulation of immunometabolism - Nature Reviews Immunology
Abstract Metabolic pathways and redox reactions are at the core of life. In the past decade(s), numerous discoveries have shed light on how metabolic pathways determine the cellular fate and function of lymphoid and myeloid cells, giving rise to an area of research referred to as immunometabolism. Upon activation, however, immune cells not only engage specific metabolic pathways but also rearrange their oxidation–reduction (redox) system, which in turn supports metabolic reprogramming.
The thioredoxin‐1 inhibitor Txnip restrains effector T cell and germinal center B cell expansion in mice
Short Communication Manfred Kopf Corresponding Author E-mail address: Manfred.Kopf@ethz.ch https://orcid.org/0000-0002-0628-7140 Institute of Molecular Health Sciences, ETH Zürich, Zürich, Switzerland, 8093 Full correspondence: Manfred Kopf, ETH Zürich, Otto‐Stern‐Weg 7, 8093 Zürich, Switzerland e‐mail: Manfred.Kopf@ethz.ch Search for more papers by this author This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting,...
Author Correction: Deciphering CD4+ T cell specificity using novel MHC–TCR chimeric receptors
Correction to: Nature Immunology https://doi.org/10.1038/s41590-019-0335-z (2019), published online 11 March 2019. In the version of this article initially published, a reference (23) was cited incorrectly and two references (below) were not included in the second sentence of the first paragraph of the second Results subsection (‘Screening for gp61 mimotopes with different functional properties’). The correct citation is as follows: “...
Deciphering CD4+ T cell specificity using novel MHC–TCR chimeric receptors
Abstract αβ T cell antigen receptors (TCRs) bind complexes of peptide and major histocompatibility complex (pMHC) with low affinity, which poses a considerable challenge for the direct identification of αβ T cell cognate peptides. Here we describe a platform for the discovery of MHC class II epitopes based on the screening of engineered reporter cells expressing novel pMHC–TCR (MCR) hybrid molecules carrying cDNA-derived peptides.
Regulatory T cells are required for normal and activin‐promoted wound repair in mice
Healing of skin wounds is orchestrated by various types of immune cells, but little is known about the role of FoxP3+ regulatory T cells (Tregs) in this process. Here, we determined if Tregs are important for wound healing in normal mice and if they contribute to the accelerated healing of mice overexpressing the growth and differentiation factor activin.
Regulatory T cells are required for normal and activin-promoted wound repair in mice
Healing of skin wounds is orchestrated by various types of immune cells, but little is known about the role of FoxP3+ regulatory T cells (Tregs) in this process. Here we determined if Tregs are important for wound healing in normal mice and if they contribute to the accelerated healing of mice overexpressing the growth and differentiation factor activin.
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