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4. C-type lectin receptors Mcl and Mincle control development of multiple sclerosis-like neuroinflammation

Author

N'diaye, Marie, Brauner, Susanna, Flytzani, Sevasti, Kular, Lara, Warnecke, Andreas, Adzemovic, Milena Z., Piket, Eliane, Min, Jin-Hong, Edwards, Will, Mela, Filia, Choi, Hoi Ying, Magg, Vera, James, Tojo, Linden, Magdalena, Reichardt, Holger M., Daws, Michael R., van Horssen, Jack, Kockum, Ingrid, Harris, Robert A., Olsson, Tomas, Guerreiro-Cacais, Andre O., and Jagodic, Maja

Subjects
Lectins -- Analysis -- Health aspects, Autoimmunity -- Analysis -- Health aspects, Multiple sclerosis -- Development and progression -- Analysis -- Health aspects, T cells -- Analysis -- Health aspects, Brain damage, Infection, Central nervous system, Encephalomyelitis, Health care industry
Abstract

Pattern recognition receptors (PRRs) are crucial for responses to infections and tissue damage; however, their role in autoimmunity is less clear. Herein we demonstrate that 2 C-type lectin receptors (CLRs) Mcl and Mincle play an important role in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Congenic rats expressing lower levels of Mcl and Mincle on myeloid cells exhibited a drastic reduction in EAE incidence. In vivo silencing of Mcl and Mincle or blockade of their endogenous ligand SAP130 revealed that these receptors' expression in the central nervous system is crucial for T cell recruitment and reactivation into a pathogenic Th17/GM-CSF phenotype. Consistent with this, we uncovered MCL- and MINCLE-expressing cells in brain lesions of MS patients and we further found an upregulation of the MCL/MINCLE signaling pathway and an increased response following MCL/MINCLE stimulation in peripheral blood mononuclear cells from MS patients. Together, these data support a role for CLRs in autoimmunity and implicate the MCL/MINCLE pathway as a potential therapeutic target in MS., Introduction Multiple sclerosis (MS), a leading cause of neurological disability in young adults, is a chronic inflammatory disease of the central nervous system (CNS) characterized by autoimmune destruction of myelin [...]

Published
2020
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5. Corrigendum: Wild-type microglia do not reverse pathology in mouse models of Rett syndrome.

Author

Wang, Jieqi, Wegener, Jan Eike, Huang, Teng-Wei, Sripathy, Smitha, De Jesus-Cortes, Hector, Xu, Pin, Tran, Stephanie, Knobbe, Whitney, Leko, Vid, Britt, Jeremiah, Starwalt, Ruth, McDaniel, Latisha, Ward, Chris S, Parra, Diana, Newcomb, Benjamin, Lao, Uyen, Nourigat, Cynthia, Flowers, David A, Cullen, Sean, Jorstad, Nikolas L, Yang, Yue, Glaskova, Lena, Vigneau, Sébastien, Kozlitina, Julia, Yetman, Michael J, Jankowsky, Joanna L, Reichardt, Sybille D, Reichardt, Holger M, Gärtner, Jutta, Bartolomei, Marisa S, Fang, Min, Loeb, Keith, Keene, C Dirk, Bernstein, Irwin, Goodell, Margaret, Brat, Daniel J, Huppke, Peter, Neul, Jeffrey L, Bedalov, Antonio, and Pieper, Andrew A

Subjects
General Science & Technology
Published
2015

6. Wild-type microglia do not reverse pathology in mouse models of Rett syndrome.

Author

Wang, Jieqi, Wegener, Jan Eike, Huang, Teng-Wei, Sripathy, Smitha, De Jesus-Cortes, Hector, Xu, Pin, Tran, Stephanie, Knobbe, Whitney, Leko, Vid, Britt, Jeremiah, Starwalt, Ruth, McDaniel, Latisha, Ward, Chris S, Parra, Diana, Newcomb, Benjamin, Lao, Uyen, Nourigat, Cynthia, Flowers, David A, Cullen, Sean, Jorstad, Nikolas L, Yang, Yue, Glaskova, Lena, Vingeau, Sébastien, Kozlitina, Julia, Yetman, Michael J, Jankowsky, Joanna L, Reichardt, Sybille D, Reichardt, Holger M, Gärtner, Jutta, Bartolomei, Marisa S, Fang, Min, Loeb, Keith, Keene, C Dirk, Bernstein, Irwin, Goodell, Margaret, Brat, Daniel J, Huppke, Peter, Neul, Jeffrey L, Bedalov, Antonio, and Pieper, Andrew A

Subjects
Microglia, Animals, Rett Syndrome, Disease Progression, Female, Male, Methyl-CpG-Binding Protein 2, General Science & Technology
Published
2015

7. β-Synuclein-reactive T cells induce autoimmune CNS grey matter degeneration

Author

Lodygin, Dmitri, Hermann, Moritz, Schweingruber, Nils, Flügel-Koch, Cassandra, Watanabe, Takashi, Schlosser, Corinna, Merlini, Arianna, Körner, Henrike, Chang, Hsin-Fang, Fischer, Henrike J., Reichardt, Holger M., Zagrebelsky, Marta, Mollenhauer, Brit, Kügler, Sebastian, Fitzner, Dirk, Frahm, Jens, Stadelmann, Christine, Haberl, Michael, Odoardi, Francesca, and Flügel, Alexander

Published
2019
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14. Glucocorticoid receptor dimers control intestinal STAT1 and TNF-induced inflammation in mice

Author

Ballegeer, Marlies, Van Looveren, Kelly, Timmermans, Steven, Eggermont, Melanie, Vandevyver, Sofie, Thery, Fabien, Dendoncker, Karen, Souffriau, Jolien, Vandewalle, Jolien, Van Wyngene, Lise, De Rycke, Riet, Takahashi, Nozomi, Vandenabeele, Peter, Tuckermann, Jan, Reichardt, Holger M., Impens, Francis, Beyaert, Rudi, De Bosscher, Karolien, Vandenbroucke, Roosmarijn E., and Libert, Claude

Subjects
Tumor necrosis factor -- Research, Inflammation -- Research, Inflammatory bowel diseases -- Drug therapy -- Research, Glucocorticoids -- Usage -- Dosage and administration, Transcription factors -- Analysis, Dexamethasone -- Dosage and administration, Health care industry
Abstract

TNF is an important mediator in numerous inflammatory diseases, e.g., in inflammatory bowel diseases (IBDs). In IBD, acute increases in TNF production can lead to disease flares. Glucocorticoids (GCs), which are steroids that bind and activate the glucocorticoid receptor (GR), are able to protect animals and humans against acute TNF-induced inflammatory symptoms. Mice with a poor transcriptional response of GR dimer-dependent target genes were studied in a model of TNF-induced lethal inflammation. In contrast to the [GR.sup.WT/WT] mice, these [GR.sup.dim/dim] mice displayed a substantial increase in TNF sensitivity and a lack of protection by the GC dexamethasone (DEX). Unchallenged [GR.sup.dim/dim] mice had a strong IFN-stimulated gene (ISG) signature, along with STAT1 upregulation and phosphorylation. This ISG signature was gut specific and, based on our studies with antibiotics, depended on the gut microbiota. GR dimers directly bound to short DNA sequences in the STAT1 promoter known as inverted repeat negative GRE (IR-nGRE) elements. Poor control of STAT1 in [GR.sup.dim/dim] mice led to failure to repress ISG genes, resulting in excessive necroptosis induction by TNF. Our findings support a critical interplay among gut microbiota, IFNs, necroptosis, and GR in both the basal response to acute inflammatory challenges and pharmacological intervention by GCs., Introduction The cytokine TNF is of great interest in biomedical research. Low but chronic expression levels of TNF have been shown to be sufficient for the development of diseases that [...]

Published
2018
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22. Publisher Correction: β-Synuclein-reactive T cells induce autoimmune CNS grey matter degeneration

Author

Lodygin, Dmitri, Hermann, Moritz, Schweingruber, Nils, Flügel-Koch, Cassandra, Watanabe, Takashi, Schlosser, Corinna, Merlini, Arianna, Körner, Henrike, Chang, Hsin-Fang, Fischer, Henrike J., Reichardt, Holger M., Zagrebelsky, Marta, Mollenhauer, Brit, Kügler, Sebastian, Fitzner, Dirk, Frahm, Jens, Stadelmann, Christine, Haberl, Michael, Odoardi, Francesca, and Flügel, Alexander

Published
2019
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26. Regeneration competent satellite cell niches in rat engineered skeletal muscle

Author

Tiburcy, Malte, Markov, Alex, Kraemer, Lena K., Christalla, Peter, Rave‐Fraenk, Margret, Fischer, Henrike J., Reichardt, Holger M., and Zimmermann, Wolfram‐Hubertus

Subjects
Drug screening, Muscle repair, Notch-signaling, Satellite cell, Skeletal muscle, Tissue engineering, Wnt-signaling, lcsh:Biology (General), Notch‐signaling, lcsh:QH301-705.5, Research Articles, Wnt‐signaling, Research Article
Abstract

Satellite cells reside in defined niches and are activated upon skeletal muscle injury to facilitate regeneration. Mechanistic studies of skeletal muscle regeneration are hampered by the inability to faithfully simulate satellite cell biology in vitro. We sought to overcome this limitation by developing tissue engineered skeletal muscle (ESM) with (1) satellite cell niches and (2) the capacity to regenerate after injury. ESMs contained quiescent Pax7‐positive satellite cells in morphologically defined niches. Satellite cells could be activated to repair (i) cardiotoxin and (ii) mechanical crush injuries. Activation of the Wnt‐pathway was essential for muscle regeneration. Finally, muscle progenitors from the engineered niche developed de novo ESM in vitro and regenerated skeletal muscle after cardiotoxin‐induced injury in vivo. We conclude that ESM with functional progenitor niches reminiscent of the in vivo satellite cell niches can be engineered in vitro. ESM may ultimately be exploited in disease modeling, drug screening, or muscle regeneration. Open-Access-Publikationsfonds 2019 peerReviewed

Published
2019

27. The Role of Glucocorticoids in Inflammatory Diseases

Author

Reichardt, Sybille D., Amouret, Agathe, Muzzi, Chiara, Vettorazzi, Sabine, Tuckermann, Jan P., Lühder, Fred, Reichardt, Holger M., and Harris, James

Subjects
Multiple Sklerose, rheumatoid arthritis, QH301-705.5, Review, Inflammatory bowel diseases, Graft versus host disease, multiple sclerosis, Models, Biological, Lungenkrankheit, Multiple sclerosis, graft-versus-host-disease, DDC 570 / Life sciences, inflammatory bowel disease, ddc:570, glucocorticoid receptor, Animals, Humans, Transplantat-Wirt-Reaktion, Rheumatoid arthritis, Biology (General), Glucocorticoids, Inflammation, Chronische Darmentzündung, Rheumatoide Arthritis, Nanopartikel, asthma, Glucocorticoids Receptors, Disease Models, Animal, Phenotype, acute lung injury, Bronchialasthma, Nanoparticles
Abstract

For more than 70 years, glucocorticoids (GCs) have been a powerful and affordable treatment option for inflammatory diseases. However, their benefits do not come without a cost, since GCs also cause side effects. Therefore, strong efforts are being made to improve their therapeutic index. In this review, we illustrate the mechanisms and target cells of GCs in the pathogenesis and treatment of some of the most frequent inflammatory disorders affecting the central nervous system, the gastrointestinal tract, the lung, and the joints, as well as graft-versus-host disease, which often develops after hematopoietic stem cell transplantation. In addition, an overview is provided of novel approaches aimed at improving GC therapy based on chemical modifications or GC delivery using nanoformulations. GCs remain a topic of highly active scientific research despite being one of the oldest class of drugs in medical use., publishedVersion

Published
2021

31. Glucocorticoids Suppress Bone Formation by Attenuating Osteoblast Differentiation via the Monomeric Glucocorticoid Receptor

Author

Rauch, Alexander, Seitz, Sebastian, Baschant, Ulrike, Schilling, Arndt F., Illing, Anett, Stride, Brenda, Kirilov, Milen, Mandic, Vice, Takacz, Andrea, Schmidt-Ullrich, Ruth, Ostermay, Susanne, Schinke, Thorsten, Spanbroek, Rainer, Zaiss, Mario M., Angel, Peter E., Lerner, Ulf H., David, Jean-Pierre, Reichardt, Holger M., Amling, Michael, Schütz, Günther, and Tuckermann, Jan P.

Published
2010
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32. Tyrphostin AG126 exerts neuroprotection in CNS inflammation by a dual mechanism

Author

Menzfeld, Christiane, John, Michael, van Rossum, Denise, Regen, Tommy, Scheffel, Jörg, Janova, Hana, Götz, Alexander, Ribes, Sandra, Nau, Roland, Borisch, Angela, Boutin, Philippe, Neumann, Konstantin, Bremes, Vanessa, Wienands, Jürgen, Reichardt, Holger M., Lühder, Fred, Tischner, Denise, Waetzig, Vicky, Herdegen, Thomas, Teismann, Peter, Greig, Iain, Müller, Michael, Pukrop, Tobias, Mildner, Alexander, Kettenmann, Helmut, Brück, Wolfgang, Prinz, Marco, Rotshenker, Shlomo, Weber, Martin S., and Hanisch, Uwe-Karsten

Published
2015
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34. A combination of fluorescent NFAT and H2B sensors uncovers dynamics of T cell activation in real time during CNS autoimmunity

Author

Lodygin, Dmitri, Odoardi, Francesca, Schlager, Christian, Korner, Henrike, Kitz, Alexandra, Nosov, Michail, Brandt, Jens van den, Reichardt, Holger M., Haberl, Michael, and Flugel, Alexander

Subjects
T cells -- Physiological aspects -- Genetic aspects -- Research, Autoimmunity -- Development and progression -- Genetic aspects -- Research, DNA binding proteins -- Physiological aspects -- Genetic aspects -- Research, Biological sciences, Health
Abstract

Multiple sclerosis is an autoimmune disease of the central nervous system (CNS) that is initiated when self-reactive T cells enter the brain and become locally activated after encountering their specific [...]

Published
2013
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39. The glucocorticoid receptor and FOXO1 synergistically activate the skeletal muscle atrophy-associated MuRF1 gene

Author

Waddell, David S., Baehr, Leslie M., van den Brandt, Jens, Johnsen, Steven A., Reichardt, Holger M., Furlow, J. David, and Bodine, Sue C.

Subjects
DNA binding proteins -- Properties, Hormone receptors -- Properties, Atrophy, Muscular -- Genetic aspects, Muscles -- Genetic aspects, Biological sciences
Abstract

The muscle specific ubiquitin E3 ligase MuRF1 has been implicated as a key regulator of muscle atrophy under a variety of conditions, such as during synthetic glucocorticoid treatment. FOXO class transcription factors have been proposed as important regulators of MuRF1 expression, but its regulation by glucocorticoids is not well understood. The MuRF1 promoter contains a near-perfect palindromic glucocorticoid response element (GRE) 200 base pairs upstream of the transcription start site. The GRE is highly conserved in the mouse, rat, and human genes along with a directly adjacent FOXO binding element (FBE). Transient transfection assays in HepG2 cells and [C.sub.2][C.sub.12] myotubes demonstrate that the MuRF1 promoter is responsive to both the dexamethasone (DEX)-activated ghicocorticoid receptor (GR) and FOXO1, whereas coexpression of GR and FOXO1 leads to a dramatic synergistic increase in reporter gene activity. Mutation of either the GRE or the FBE significantly impairs activation of the MuRF1 promoter. Consistent with these findings, DEX-induced upregulation of MuRF1 is significantly attenuated in mice expressing a homodimerization-deficient GR despite no effect on the degree of muscle loss in these mice vs. their wild-type counterparts. Finally, chromatin immunoprecipitation analysis reveals that both GR and FOXO1 bind to the endogenous MuRF1 promoter in [C.sub.2][C.sub.12] myotubes, and IGF-I inhibition of DEX-induced MuRF1 expression correlates with the loss of FOXO1 binding. These findings present new insights into the role of the GR and FOXO family of transcription factors in the transcriptional regulation of the MuRF1 gene, a direct target of the GR in skeletal muscle. forkhead transcription factor class O; muscle RING finger 1; glucocorticoid receptor

Published
2008

40. A CD28 superagonistic antibody elicits 2 functionally distinct waves of T cell activation in rats

Author

Muller, Nora, van den Brandt, Jens, Odoardi, Francesca, Tischner, Denise, Herath, Judith, Flugel, Alexander, and Reichardt, Holger M.

Subjects
CD8 lymphocytes -- Properties, Antibodies -- Properties, Viral antibodies -- Properties
Abstract

Administration of the CD28 superagonistic antibody JJ316 is an efficient means to treat autoimmune diseases in rats, but the humanized antibody TGN1412 caused devastating side effects in healthy volunteers during a clinical trial. Here we show that JJ316 treatment of rats induced a dramatic redistribution of T lymphocytes from the periphery to the secondary lymphoid organs, resulting in severe T lymphopenia. Live imaging of secondary lymphoid organs revealed that JJ316 administration almost instantaneously (, Introduction Efficient activation of naive T cells by antigen-presenting cells requires the concomitant engagement of the TCR and the costimulatory molecule CD28 (1). These 2 signals result in an upregulation [...]

Published
2008

41. Macrophages and neutrophils are the targets for immune suppression by glucocorticoids in contact allergy

Author

Tuckermann, Jan P., Kleiman, Anna, Moriggl, Richard, Spanbroek, Rainer, Neumann, Anita, Illing, Anett, Clausen, Bjorn E., Stride, Brenda, Forster, Irmgard, Habenicht, Andreas J.R., Reichardt, Holger M., Tronche, Francois, Schmid, Wolfgang, and Schutz, Gunther

Subjects
Contact dermatitis -- Drug therapy, Corticosteroids -- Dosage and administration, Corticosteroids -- Complications and side effects, Macrophages -- Health aspects, Neutrophils -- Health aspects
Abstract

Glucocorticoids (GCs) are widely used in the treatment of allergic skin conditions despite having numerous side effects. Here we use Cre/loxP-engineered tissue- and cell-specific and function-selective GC receptor (GR) mutant [...]

Published
2007

42. The glucocorticoid receptor in recipient cells keeps cytokine secretion in acute graft-versus-host disease at bay

Author

Baake, Tina, Jörß, Katharina, Suennemann, Jennifer, Roßmann, Laura, Bohnenberger, Hanibal, Tuckermann, Jan P., Reichardt, Holger M., Fischer, Henrike J., and Reichardt, Sybille D.

Subjects
GvHD, IL-6, surgical procedures, operative, myeloid cells, cytokine storm, Research Paper: Immunology, glucocorticoid receptor
Abstract

Graft-versus-host disease (GvHD) is a life-threatening complication of hematopoietic stem cell transplantation (HSCT), which is caused by allogeneic T cells recognizing molecules of the recipient as foreign. Endogenous glucocorticoids (GC) released from the adrenal gland are crucial in regulating such inflammatory diseases. Here we demonstrate that genetically engineered mice, that are largely unresponsive to GC, suffer from aggravated clinical symptoms and increased mortality after HSCT, effects that could be tempered by neutralization of IL-6. Interestingly, selective ablation of the GC receptor (GR) in recipient myeloid cells resulted in fulminant disease as well. While histopathological analysis of the jejunum failed to reveal any differences between sick mice of both genotypes, systemic IL-6 and TNFα secretion was strongly increased in transplanted mice lacking the GR in myeloid cells briefly before the majority of them succumbed to the disease. Collectively, our findings reveal an important role of the GR in recipient cells in limiting the cytokine storm caused by GvHD induction.

Published
2018

45. C-type lectin receptors Mcl and Mincle control development of multiple sclerosis–like neuroinflammation

Author

N’diaye, Marie, primary, Brauner, Susanna, additional, Flytzani, Sevasti, additional, Kular, Lara, additional, Warnecke, Andreas, additional, Adzemovic, Milena Z., additional, Piket, Eliane, additional, Min, Jin-Hong, additional, Edwards, Will, additional, Mela, Filia, additional, Choi, Hoi Ying, additional, Magg, Vera, additional, James, Tojo, additional, Linden, Magdalena, additional, Reichardt, Holger M., additional, Daws, Michael R., additional, van Horssen, Jack, additional, Kockum, Ingrid, additional, Harris, Robert A., additional, Olsson, Tomas, additional, Guerreiro-Cacais, Andre O., additional, and Jagodic, Maja, additional

Published
2020
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46. Glucocorticoid resistance of allogeneic T cells alters the gene expression profile in the inflamed small intestine of mice suffering from acute graft-versus-host disease

Author

Li, Hu, primary, Kaiser, Tina K., additional, Borschiwer, Marina, additional, Bohnenberger, Hanibal, additional, Reichardt, Sybille D., additional, Lühder, Fred, additional, Walter, Lutz, additional, Dressel, Ralf, additional, Meijsing, Sebastiaan H., additional, and Reichardt, Holger M., additional

Published
2019
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47. The glucocorticoid receptor is required for stress erythropoiesis

Author

Bauer, Anton, Tronche, Francois, Wessely, Oliver, Kellendonk, Christoph, Reichardt, Holger M., Steinlein, Peter, Schutz, Gunther, and Beug, Harmut

Subjects
Cytochemistry -- Research, Adrenocortical hormones -- Research, Hormone receptors -- Physiological aspects, Erythropoiesis -- Regulation, Stress (Physiology) -- Research, Biological sciences
Abstract

The glucocorticoid receptor (GR) has been shown to be necessary for stress erythropoiesis, which requires GR-mediated regulation of erythroid progenitor (ebl) proliferation. The impact of the GR on erythropoiesis in vivo has been studied using GR-deficient mice or those expressing a GR defective for transactivation. Mice lacking the GR die at birth so fetal livers were used after onset of definitive erythropoiesis at E14.5. In vitro sustained primary ebls proliferation must have intact GR.

Published
1999

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