Hannah Theobald

University of Bonn

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Andreas Schlitzer

University of Bonn

Marc Beyer

German Center for Neurodegenerative Diseases

Florent Ginhoux

Singapore Immunology Network

Waldemar Kolanus

University of Bonn

Amirah Al Jawazneh

Bernhard Nocht Institute for Tropical Medicine

Jessica Haub

University of Bonn

Federica Piattini

ETH Zurich

Kristian Haendler

Epigenomics (Germany)

Xiang Yu

Shanghai Jiao Tong University

Tobias Beckröge

Life & Brain (Germany)

Cooperative Institutions

University of Bonn

KU Leuven

Life & Brain (Germany)

Universität Innsbruck

Johannes Gutenberg University Mainz

University Medical Center of the Johannes Gutenberg University Mainz

Innsbruck Medical University

German Center for Neurodegenerative Diseases

Friedrich-Alexander-Universität Erlangen-Nürnberg

Universitätsklinikum Erlangen

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Apolipoprotein E controls Dectin-1-dependent development of monocyte-derived alveolar macrophages upon pulmonary β-glucan-induced inflammatory adaptation

bioRxiv (Cold Spring Harbor Laboratory) (2022)

Hannah Theobald David Alejandro Bejarano Natalie Katzmarski Jessica Haub Jonas Schulte-Schrepping

Summary The lung is constantly exposed to the outside world and optimal adaptation of immune responses is crucial for efficient pathogen clearance. However, mechanisms which lead to the functional and developmental adaptation of lung-associated macrophages remain elusive. To reveal such mechanisms, we developed a reductionist model of environmental intranasal β-glucan exposure, allowing for the detailed interrogation of molecular mechanisms of pulmonal macrophage adaptation. Employing single-cell transcriptomics, high dimensional imaging and flow cytometric characterization paired to in vivo and ex vivo challenge models, we reveal that pulmonary low-grade inflammation results in the development of Dectin-1 - Card9 signaling-dependent monocyte-derived macrophages (MoAM). MoAMs expressed high levels of CD11b, ApoE, Gpnmb and Ccl6, were glycolytic and produced large amounts of interleukin 6 upon restimulation. Myeloid cell specific ApoE ablation inhibited monocyte to MoAM differentiation dependent on M-CSF secretion, promoting MoAM cell death thus impeding MoAM maintenance. In vivo , β-glucan-elicited MoAMs limited the bacterial burden of Legionella pneumophilia post infection and ameliorated fibrosis severity in a murine fibrosis model. Collectively these data identify MoAMs that are generated upon environmental cues and ApoE as an important determinant for lung immune resilience.

Ex vivo

Monocyte

Alveolar macrophage

10.1101/2022.09.15.505390

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Impaired primitive erythropoiesis and defective vascular development in Trim71-KO embryos

Life Science Alliance (2025)

Tobias Beckröge Bettina Jux Hannah Seifert Hannah Theobald Elena De Domenico

The transition of an embryo from gastrulation to organogenesis requires precisely coordinated changes in gene expression, but the underlying mechanisms remain unclear. The RNA-binding protein Trim71 is essential for development and serves as a potent regulator of post-transcriptional gene expression. Here, we show that global deficiency of Trim71 induces severe defects in mesoderm-derived cells at the onset of organogenesis. Murine Trim71 -KO embryos displayed impaired primitive erythropoiesis, yolk sac vasculature, heart function, and circulation, explaining the embryonic lethality of these mice. Tie2 Cre Trim71 conditional knockout did not induce strong defects, showing that Trim71 expression in endothelial cells and their immediate progenitors is dispensable for embryonic survival. scRNA-seq of E7.5 global Trim71 -KO embryos revealed that transcriptomic changes arise already at gastrulation, showing a strong up-regulation of the mesodermal pioneer transcription factor Eomes. We identify Eomes as a direct target of Trim71-mediated mRNA repression via the NHL domain, demonstrating a functional link between these important regulatory genes. Taken together, our data suggest that Trim71-dependent control of gene expression at gastrulation establishes a framework for proper development during organogenesis.

Organogenesis

Brachyury

10.26508/lsa.202402956

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Guidelines for DC preparation and flow cytometry analysis of mouse nonlymphoid tissues

European Journal of Immunology (2022)

Hans Christian Probst Patrizia Stoitzner Lukas Amon Ronald A. Backer Anna Brand

Abstract This article is part of the Dendritic Cell Guidelines article series, which provides a collection of state‐of‐the‐art protocols for the preparation, phenotype analysis by flow cytometry, generation, fluorescence microscopy and functional characterization of mouse and human dendritic cells (DC) from lymphoid organs and various nonlymphoid tissues. DC are sentinels of the immune system present in almost every mammalian organ. Since they represent a rare cell population, DC need to be extracted from organs with protocols that are specifically developed for each tissue. This article provides detailed protocols for the preparation of single‐cell suspensions from various mouse nonlymphoid tissues, including skin, intestine, lung, kidney, mammary glands, oral mucosa and transplantable tumors. Furthermore, our guidelines include comprehensive protocols for multiplex flow cytometry analysis of DC subsets and feature top tricks for their proper discrimination from other myeloid cells. With this collection, we provide guidelines for in‐depth analysis of DC subsets that will advance our understanding of their respective roles in healthy and diseased tissues. While all protocols were written by experienced scientists who routinely use them in their work, this article was also peer‐reviewed by leading experts and approved by all coauthors, making it an essential resource for basic and clinical DC immunologists.

Cytometry

10.1002/eji.202249819

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Dedicated macrophages organize and maintain the enteric nervous system

Nature (2023)

Maria Francesca Viola Marta Chavero‐Pieres Elodie Modave Marcello Delfini Nathalie Stakenborg

Enteric Nervous System

10.1038/s41586-023-06200-7

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Citations (51)

Dysregulation of gene expression during gastrulation results in impaired primitive erythropoiesis and vascular development in Trim71-KO embryos

bioRxiv (Cold Spring Harbor Laboratory) (2024)

Tobias Beckröge Bettina Jux Hannah Seifert Hannah Theobald Elena De Domenico

Abstract The transition of an embryo from gastrulation to organogenesis requires precisely coordinated changes in gene expression. The RNA-binding protein Trim71 is essential for embryonic survival, but its exact role in mammalian development in vivo remains poorly defined. Here we show that murine Trim71 -KO embryos appear normal until embryonic day (E)8.5 but display severe defects in primitive erythropoiesis, yolk sac vasculature and heart function during the onset of organogenesis at E9.5 and E10.5. This led to an impaired vascular translocation of yolk sac-derived macrophage progenitors to the embryo head, independent of Trim71 expression in erythro-myeloid progenitors. The cardiovascular and erythropoiesis defects explain the embryonic lethality upon global Trim71 -KO. Targeting Trim71 in hematoendothelial progenitors did not induce strong developmental defects, indicating an earlier developmental origin of these phenotypes in Trim71 -KO embryos. ScRNA-seq of E7.5 Trim71 -KO embryos revealed that transcriptomic changes arise already at gastrulation, showing a strong upregulation of the transcription factor Eomes. We identify Eomes as a direct target of Trim71-mediated mRNA repression via the NHL domain, demonstrating a functional link of Trim71 to a key regulator of mesodermal development. Taken together, our data suggest that Trim71-dependent control of gene expression at gastrulation establishes a framework for proper development during organogenesis.

10.1101/2024.07.12.603214

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Citations (1)

Apolipoprotein E controls Dectin-1-dependent development of monocyte-derived alveolar macrophages upon pulmonary β-glucan-induced inflammatory adaptation

Nature Immunology (2024)

Hannah Theobald David Alejandro Bejarano Natalie Katzmarski Jessica Haub Jonas Schulte-Schrepping

The lung is constantly exposed to the outside world and optimal adaptation of immune responses is crucial for efficient pathogen clearance. However, mechanisms that lead to lung-associated macrophages' functional and developmental adaptation remain elusive. To reveal such mechanisms, we developed a reductionist model of environmental intranasal β-glucan exposure, allowing for the detailed interrogation of molecular mechanisms of pulmonary macrophage adaptation. Employing single-cell transcriptomics, high-dimensional imaging and flow cytometric characterization paired with in vivo and ex vivo challenge models, we reveal that pulmonary low-grade inflammation results in the development of apolipoprotein E (ApoE)-dependent monocyte-derived alveolar macrophages (ApoE

Monocyte

Alveolar macrophage

Ex vivo

Apolipoprotein E

10.1038/s41590-024-01830-z

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Citations (10)