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1. Molecular anatomy of adult mouse leptomeninges

Author

Pietilä, Riikka, Del Gaudio, Francesca, He, Liqun, Vázquez-Liébanas, Elisa, Vanlandewijck, Michael, Muhl, Lars, Mocci, Giuseppe, Bjørnholm, Katrine D, Lindblad, Caroline, Fletcher-Sandersjöö, Alexander, Svensson, Mikael, Thelin, Eric P, Liu, Jianping, van Voorden, A Jantine, Torres, Monica, Antila, Salli, Xin, Li, Karlström, Helena, Storm-Mathisen, Jon, Bergersen, Linda Hildegard, Moggio, Aldo, Hansson, Emil M, Ulvmar, Maria H, Nilsson, Per, Mäkinen, Taija, Andaloussi Mäe, Maarja, Alitalo, Kari, Proulx, Steven T, Engelhardt, Britta, McDonald, Donald M, Lendahl, Urban, Andrae, Johanna, and Betsholtz, Christer

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Brain Disorders, Physical Injury - Accidents and Adverse Effects, Underpinning research, 1.1 Normal biological development and functioning, Mice, Animals, Meninges, Arachnoid, Pia Mater, Choroid Plexus, Brain, arachnoid barrier, arachnoid mater, brain fibroblasts, dura mater, leptomeninges, perivascular fibroblast, pia mater, single-cell RNA sequencing, traumatic brain injury, tricellular junction, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

Leptomeninges, consisting of the pia mater and arachnoid, form a connective tissue investment and barrier enclosure of the brain. The exact nature of leptomeningeal cells has long been debated. In this study, we identify five molecularly distinct fibroblast-like transcriptomes in cerebral leptomeninges; link them to anatomically distinct cell types of the pia, inner arachnoid, outer arachnoid barrier, and dural border layer; and contrast them to a sixth fibroblast-like transcriptome present in the choroid plexus and median eminence. Newly identified transcriptional markers enabled molecular characterization of cell types responsible for adherence of arachnoid layers to one another and for the arachnoid barrier. These markers also proved useful in identifying the molecular features of leptomeningeal development, injury, and repair that were preserved or changed after traumatic brain injury. Together, the findings highlight the value of identifying fibroblast transcriptional subsets and their cellular locations toward advancing the understanding of leptomeningeal physiology and pathology.

Published
2023

2. VE-cadherin in arachnoid and pia mater cells serves as a suitable landmark for in vivo imaging of CNS immune surveillance and inflammation.

Author

Mapunda, Josephine, Pareja, Javier, Vladymyrov, Mykhailo, Bouillet, Elisa, Hélie, Pauline, Pleskač, Petr, Barcos, Sara, Andrae, Johanna, Vestweber, Dietmar, McDonald, Donald, Betsholtz, Christer, Deutsch, Urban, Proulx, Steven, and Engelhardt, Britta

Subjects
Female, Animals, Mice, Pia Mater, Neuroinflammatory Diseases, Central Nervous System, Arachnoid, Cadherins, Inflammation, Mice, Transgenic
Abstract

Meninges cover the surface of the brain and spinal cord and contribute to protection and immune surveillance of the central nervous system (CNS). How the meningeal layers establish CNS compartments with different accessibility to immune cells and immune mediators is, however, not well understood. Here, using 2-photon imaging in female transgenic reporter mice, we describe VE-cadherin at intercellular junctions of arachnoid and pia mater cells that form the leptomeninges and border the subarachnoid space (SAS) filled with cerebrospinal fluid (CSF). VE-cadherin expression also marked a layer of Prox1+ cells located within the arachnoid beneath and separate from E-cadherin+ arachnoid barrier cells. In vivo imaging of the spinal cord and brain in female VE-cadherin-GFP reporter mice allowed for direct observation of accessibility of CSF derived tracers and T cells into the SAS bordered by the arachnoid and pia mater during health and neuroinflammation, and detection of volume changes of the SAS during CNS pathology. Together, the findings identified VE-cadherin as an informative landmark for in vivo imaging of the leptomeninges that can be used to visualize the borders of the SAS and thus potential barrier properties of the leptomeninges in controlling access of immune mediators and immune cells into the CNS during health and neuroinflammation.

Published
2023

3. Inflammation-induced TRPV4 channels exacerbate blood–brain barrier dysfunction in multiple sclerosis

Author

Hansen, Cathrin E., Kamermans, Alwin, Mol, Kevin, Berve, Kristina, Rodriguez-Mogeda, Carla, Fung, Wing Ka, van het Hof, Bert, Fontijn, Ruud D., van der Pol, Susanne M. A., Michalick, Laura, Kuebler, Wolfgang M., Kenkhuis, Boyd, van Roon-Mom, Willeke, Liedtke, Wolfgang, Engelhardt, Britta, Kooij, Gijs, Witte, Maarten E., and de Vries, Helga E.

Published
2024
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11. A20 regulates lymphocyte adhesion in murine neuroinflammation by restricting endothelial ICOSL expression in the CNS

Author

Johann, Lisa, Soldati, Sasha, Muller, Kristin, Lampe, Josephine, Marini, Federico, Klein, Matthias, Schramm, Eva, Ries, Nathalie, Schelmbauer, Carsten, Palagi, Ilaria, Karram, Khalad, Assmann, Julian C., Khan, Mahtab A., Wenzel, Jan, Schmidt, Mirko H.H., Korbelin, Jakob, Schluter, Dirk, van Loo, Geert, Bopp, Tobias, Engelhardt, Britta, Schwaninger, Markus, and Waisman, Ari

Subjects
T cells -- Analysis, Multiple sclerosis -- Analysis, Endothelium -- Analysis, B cells -- Analysis, Health care industry
Abstract

A20 is a ubiquitin-modifying protein that negatively regulates NF-[kappa]B signaling. Mutations in A20/TNFAIP3 are associated with a variety of autoimmune diseases, including multiple sclerosis (MS). We found that deletion of A20 in central nervous system (CNS) endothelial cells (ECs) enhances experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. [A20.sup.[DELTA]CNS-EC] mice showed increased numbers of CNS-infiltrating immune cells during neuroinflammation and in the steady state. While the integrity of the blood-brain barrier (BBB) was not impaired, we observed a strong activation of CNS- ECs in these mice, with dramatically increased levels of the adhesion molecules ICAM-1 and VCAM-1. We discovered ICOSL to be expressed by A20-deficient CNS-ECs, which we found to function as adhesion molecules. Silencing of ICOSL in CNS microvascular ECs partly reversed the phenotype of [A20.sup.[DELTA]CNS-EC] mice without reaching statistical significance and delayed the onset of EAE symptoms in WT mice. In addition, blocking of ICOSL on primary mouse brain microvascular ECs impaired the adhesion of T cells in vitro. Taken together, we propose that CNS EC-ICOSL contributes to the firm adhesion of T cells to the BBB, promoting their entry into the CNS and eventually driving neuroinflammation., Introduction Multiple sclerosis (MS) is the most prevalent chronic inflammatory disease of the central nervous system (CNS) in young adults (1). To date, the causes of MS are not fully [...]

Published
2023
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14. Brain Barriers and Multiple Sclerosis: Novel Treatment Approaches from a Brain Barriers Perspective

Author

Nishihara, Hideaki, Engelhardt, Britta, Barrett, James E., Editor-in-Chief, Flockerzi, Veit, Editorial Board Member, Frohman, Michael A., Editorial Board Member, Geppetti, Pierangelo, Editorial Board Member, Hofmann, Franz B., Editorial Board Member, Kuner, Rohini, Editorial Board Member, Michel, Martin C., Editorial Board Member, Page, Clive P., Editorial Board Member, Wang, KeWei, Editorial Board Member, Cader, Zameel, editor, and Neuhaus, Winfried, editor

Published
2022
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15. Guidelines for the use of flow cytometry and cell sorting in immunological studies (second edition)

Author

Cossarizza, Andrea, Chang, Hyun-Dong, Radbruch, Andreas, Acs, Andreas, Adam, Dieter, Adam-Klages, Sabine, Agace, William W, Aghaeepour, Nima, Akdis, Mübeccel, Allez, Matthieu, Almeida, Larissa Nogueira, Alvisi, Giorgia, Anderson, Graham, Andrä, Immanuel, Annunziato, Francesco, Anselmo, Achille, Bacher, Petra, Baldari, Cosima T, Bari, Sudipto, Barnaba, Vincenzo, Barros-Martins, Joana, Battistini, Luca, Bauer, Wolfgang, Baumgart, Sabine, Baumgarth, Nicole, Baumjohann, Dirk, Baying, Bianka, Bebawy, Mary, Becher, Burkhard, Beisker, Wolfgang, Benes, Vladimir, Beyaert, Rudi, Blanco, Alfonso, Boardman, Dominic A, Bogdan, Christian, Borger, Jessica G, Borsellino, Giovanna, Boulais, Philip E, Bradford, Jolene A, Brenner, Dirk, Brinkman, Ryan R, Brooks, Anna ES, Busch, Dirk H, Büscher, Martin, Bushnell, Timothy P, Calzetti, Federica, Cameron, Garth, Cammarata, Ilenia, Cao, Xuetao, Cardell, Susanna L, Casola, Stefano, Cassatella, Marco A, Cavani, Andrea, Celada, Antonio, Chatenoud, Lucienne, Chattopadhyay, Pratip K, Chow, Sue, Christakou, Eleni, Čičin-Šain, Luka, Clerici, Mario, Colombo, Federico S, Cook, Laura, Cooke, Anne, Cooper, Andrea M, Corbett, Alexandra J, Cosma, Antonio, Cosmi, Lorenzo, Coulie, Pierre G, Cumano, Ana, Cvetkovic, Ljiljana, Dang, Van Duc, Dang-Heine, Chantip, Davey, Martin S, Davies, Derek, De Biasi, Sara, Del Zotto, Genny, Dela Cruz, Gelo Victoriano, Delacher, Michael, Della Bella, Silvia, Dellabona, Paolo, Deniz, Günnur, Dessing, Mark, Di Santo, James P, Diefenbach, Andreas, Dieli, Francesco, Dolf, Andreas, Dörner, Thomas, Dress, Regine J, Dudziak, Diana, Dustin, Michael, Dutertre, Charles-Antoine, Ebner, Friederike, Eckle, Sidonia BG, Edinger, Matthias, Eede, Pascale, Ehrhardt, Götz RA, Eich, Marcus, Engel, Pablo, Engelhardt, Britta, and Erdei, Anna

Subjects
1.1 Normal biological development and functioning, Underpinning research, Inflammatory and immune system, Allergy and Immunology, Cell Separation, Consensus, Flow Cytometry, Humans, Phenotype, Immunology
Abstract

These guidelines are a consensus work of a considerable number of members of the immunology and flow cytometry community. They provide the theory and key practical aspects of flow cytometry enabling immunologists to avoid the common errors that often undermine immunological data. Notably, there are comprehensive sections of all major immune cell types with helpful Tables detailing phenotypes in murine and human cells. The latest flow cytometry techniques and applications are also described, featuring examples of the data that can be generated and, importantly, how the data can be analysed. Furthermore, there are sections detailing tips, tricks and pitfalls to avoid, all written and peer-reviewed by leading experts in the field, making this an essential research companion.

Published
2019

17. The heavy subunit of ferritin stimulates NLRP3 inflammasomes in hepatic stellate cells through ICAM-1 to drive hepatic inflammation

Author

Fernandez-Rojo, Manuel A., primary, Pearen, Michael A., additional, Burgess, Anita G., additional, Ikonomopoulou, Maria P., additional, Hoang-Le, Diem, additional, Genz, Berit, additional, Saggiomo, Silvia L., additional, Nawaratna, Sujeevi S. K., additional, Poli, Maura, additional, Reissmann, Regina, additional, Gobert, Geoffrey N., additional, Deutsch, Urban, additional, Engelhardt, Britta, additional, Brooks, Andrew J., additional, Jones, Alun, additional, Arosio, Paolo, additional, and Ramm, Grant A., additional

Published
2024
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24. Neutrophil recruitment limited by high-affinity bent β2 integrin binding ligand in cis.

Author

Fan, Zhichao, McArdle, Sara, Marki, Alex, Mikulski, Zbigniew, Gutierrez, Edgar, Engelhardt, Britta, Deutsch, Urban, Ginsberg, Mark, Groisman, Alex, and Ley, Klaus

Subjects
Neutrophils, Animals, Mice, Inbred C57BL, Transplantation Chimera, Mice, Knockout, Humans, Mice, Inflammation, Cell Adhesion Molecules, Recombinant Proteins, Ligands, Imaging, Three-Dimensional, Bone Marrow Transplantation, Neutrophil Infiltration, Protein Conformation, Protein Binding, Stereoisomerism, Male, Molecular Imaging, Healthy Volunteers, Intravital Microscopy, CD18 Antigens, Imaging, Three-Dimensional, Inbred C57BL, Knockout
Abstract

Neutrophils are essential for innate immunity and inflammation and many neutrophil functions are β2 integrin-dependent. Integrins can extend (E(+)) and acquire a high-affinity conformation with an 'open' headpiece (H(+)). The canonical switchblade model of integrin activation proposes that the E(+) conformation precedes H(+), and the two are believed to be structurally linked. Here we show, using high-resolution quantitative dynamic footprinting (qDF) microscopy combined with a homogenous conformation-reporter binding assay in a microfluidic device, that a substantial fraction of β2 integrins on human neutrophils acquire an unexpected E(-)H(+) conformation. E(-)H(+) β2 integrins bind intercellular adhesion molecules (ICAMs) in cis, which inhibits leukocyte adhesion in vitro and in vivo. This endogenous anti-inflammatory mechanism inhibits neutrophil aggregation, accumulation and inflammation.

Published
2016

25. Compromised Blood-Brain Barrier Junctions Enhance Melanoma Cell Intercalation and Extravasation

Author

Saltarin, Federico, primary, Wegmüller, Adrian, additional, Bejarano, Leire, additional, Ildiz, Ece Su, additional, Zwicky, Pascale, additional, Vianin, Andréj, additional, Spadin, Florentin, additional, Soukup, Klara, additional, Wischnewski, Vladimir, additional, Engelhardt, Britta, additional, Deutsch, Urban, additional, J. Marques, Ines, additional, Frenz, Martin, additional, Joyce, Johanna A., additional, and Lyck, Ruth, additional

Published
2023
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27. Angiopoietin-2 blockade ameliorates autoimmune neuroinflammation by inhibiting leukocyte recruitment into the CNS

Author

Li, Zhilin, Korhonen, Emilia A., Merlini, Arianna, Strauss, Judith, Wihuri, Eleonoora, Nurmi, Harri, Antila, Salli, Paech, Jennifer, Deutsch, Urban, Engelhardt, Britta, Chintharlapalli, Sudhakar, Koh, Gou Young, Flugel, Alexander, and Alitalo, Kari

Subjects
R and D Systems, Genetic engineering -- Analysis, Tetracyclines -- Analysis, Macrophages -- Analysis, Autoimmunity -- Analysis, Inflammation -- Development and progression, Software industry -- Analysis, Integrins -- Analysis, Multiple sclerosis -- Development and progression, Antigens, Phenols (Class of compounds), Diseases, Tyrosine, Genes, Endothelium, Autoimmune diseases, Central nervous system, Encephalomyelitis, Health care industry
Abstract

Angiopoietin-2 (Ang2), a ligand of the endothelial Tie2 tyrosine kinase, is involved in vascular inflammation and leakage in critically ill patients. However, the role of Ang2 in demyelinating central nervous system (CNS) autoimmune diseases is unknown. Here, we report that Ang2 is critically involved in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), a rodent model of multiple sclerosis. Ang2 expression was induced in CNS autoimmunity, and transgenic mice overexpressing Ang2 specifically in endothelial cells (ECs) developed a significantly more severe EAE. In contrast, treatment with Ang2-blocking Abs ameliorated neuroinflammation and decreased spinal cord demyelination and leukocyte infiltration into the CNS. Similarly, Ang2-binding and Tie2-activating Ab attenuated the development of CNS autoimmune disease. Ang2 blockade inhibited expression of EC adhesion molecules, improved blood-brain barrier integrity, and decreased expression of genes involved in antigen presentation and proinflammatory responses of microglia and macrophages, which was accompanied by inhibition of [[alpha].sub.5][[beta].sub.1] integrin activation in microglia. Taken together, our data suggest that Ang2 provides a target for increasing Tie2 activation in ECs and inhibiting proinflammatory polarization of CNS myeloid cells via [[alpha].sub.5][[beta].sub.1] integrin in neuroinflammation. Thus, Ang2 targeting may serve as a therapeutic option for the treatment of CNS autoimmune disease., Introduction The blood-brain barrier (BBB) is indispensable for the maintenance of CNS homeostasis, acting by restricting molecular and cellular trafficking across the blood vascular endothelium into the CNS (1). Compromised [...]

Published
2020
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33. Dual role of ALCAM in neuroinflammation and blood—brain barrier homeostasis

Author

Lécuyer, Marc-André, Saint-Laurent, Olivia, Bourbonnière, Lyne, Larouche, Sandra, Larochelle, Catherine, Michel, Laure, Charabati, Marc, Abadier, Michael, Zandee, Stephanie, Jahromi, Neda Haghayegh, Gowing, Elizabeth, Pittet, Camille, Lyck, Ruth, Engelhardt, Britta, and Prat, Alexandre

Published
2017

36. Effects of a Small-Molecule Perforin Inhibitor in a Mouse Model of CD8 T Cell–Mediated Neuroinflammation

Author

Gonzalez-Fierro, Carmen, primary, Fonte, Coralie, additional, Dufourd, Eloïse, additional, Cazaentre, Vincent, additional, Aydin, Sidar, additional, Engelhardt, Britta, additional, Caspi, Rachel R., additional, Xu, Biying, additional, Martin-Blondel, Guillaume, additional, Spicer, Julie A., additional, Trapani, Joseph A., additional, Bauer, Jan, additional, Liblau, Roland S., additional, and Bost, Chloé, additional

Published
2023
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44. Differentiation of Human Induced Pluripotent Stem Cells to Brain Microvascular Endothelial Cell-Like Cells with a Mature Immune Phenotype

Author

Matsuo, Kinya, Engelhardt, Britta, and Nishihara, Hideaki

Subjects
General Immunology and Microbiology, General Chemical Engineering, General Neuroscience, 610 Medicine & health, General Biochemistry, Genetics and Molecular Biology
Abstract

Blood-brain barrier (BBB) dysfunction is a pathological hallmark of many neurodegenerative and neuroinflammatory diseases affecting the central nervous system (CNS). Due to the limited access to disease-related BBB samples, it is still not well understood whether BBB malfunction is causative for disease development or rather a consequence of the neuroinflammatory or neurodegenerative process. Human induced pluripotent stem cells (hiPSCs) therefore provide a novel opportunity to establish in vitro BBB models from healthy donors and patients, and thus to study disease-specific BBB characteristics from individual patients. Several differentiation protocols have been established for deriving brain microvascular endothelial cell (BMEC)-like cells from hiPSCs. Consideration of the specific research question is mandatory for the correct choice of the respective BMEC-differentiation protocol. Here, we describe the extended endothelial cell culture method (EECM), which is optimized to differentiate hiPSCs into BMEC-like cells with a mature immune phenotype, allowing the study of immune cell-BBB interactions. In this protocol, hiPSCs are first differentiated into endothelial progenitor cells (EPCs) by activating Wnt/β-catenin signaling. The resulting culture, which contains smooth muscle-like cells (SMLCs), is then sequentially passaged to increase the purity of endothelial cells (ECs) and to induce BBB-specific properties. Co-culture of EECM-BMECs with these SMLCs or conditioned medium from SMLCs allows for the reproducible, constitutive, and cytokine-regulated expression of EC adhesion molecules. Importantly, EECM-BMEC-like cells establish barrier properties comparable to primary human BMECs, and due to their expression of all EC adhesion molecules, EECM-BMEC-like cells are different from other hiPSC-derived in vitro BBB models. EECM-BMEC-like cells are thus the model of choice for investigating the potential impact of disease processes at the level of the BBB, with an impact on immune cell interaction in a personalized fashion.

Published
2023

45. Blockade of VEGFR3 signaling leads to functional impairment of dural lymphatic vessels without affecting autoimmune neuroinflammation

Author

Li, Zhilin, Antila, Salli, Nurmi, Harri, Chilov, Dmitri, Korhonen, Emilia A, Fang, Shentong, Karaman, Sinem, Engelhardt, Britta, Alitalo, Kari, Research Programs Unit, and CAN-PRO - Translational Cancer Medicine Program

Subjects
Immunology, General Medicine, 3111 Biomedicine, 610 Medicine & health
Abstract

This is the author's version of the work. It is posted here by permission of the AAAS for personal use, not for redistribution. The definitive version was published in Science Immunology 8, (2023-04-14), doi: 10.1126/sciimmunol.abq0375. The recent discovery of lymphatic vessels (LVs) in the dura mater, the outermost layer of meninges around the central nervous system (CNS), has opened a possibility for the development of alternative therapeutics for CNS disorders. The vascular endothelial growth factor C (VEGF-C)/VEGF receptor 3 (VEGFR3) signaling pathway is essential for the development and maintenance of dural LVs. However, its significance in mediating dural lymphatic function in CNS autoimmunity is unclear. We show that inhibition of the VEGF-C/VEGFR3 signaling pathway using a monoclonal VEGFR3-blocking antibody, a soluble VEGF-C/D trap, or deletion of the Vegfr3 gene in adult lymphatic endothelium causes notable regression and functional impairment of dural LVs but has no effect on the development of CNS autoimmunity in mice. During autoimmune neuroinflammation, the dura mater was only minimally affected, and neuroinflammation-induced helper T (TH) cell recruitment, activation, and polarization were significantly less pronounced in the dura mater than in the CNS. In support of this notion, during autoimmune neuroinflammation, blood vascular endothelial cells in the cranial and spinal dura expressed lower levels of cell adhesion molecules and chemokines, and antigen-presenting cells (i.e., macrophages and dendritic cells) had lower expression of chemokines, MHC class II–associated molecules, and costimulatory molecules than their counterparts in the brain and spinal cord, respectively. The significantly weaker TH cell responses in the dura mater may explain why dural LVs do not contribute directly to CNS autoimmunity.

Published
2023

48. Autoimmune neuroinflammation triggers mitochondrial oxidation in oligodendrocytes

Author

Steudler, Jasmin, Ecott, Timothy, Ivan, Daniela C, Bouillet, Elisa, Walthert, Sabrina, Berve, Kristina, Dick, Tobias P, Engelhardt, Britta, and Locatelli, Giuseppe

Subjects
Encephalomyelitis, Autoimmune, Experimental, Multiple Sclerosis, genetic structures, fungi, 610 Medicine & health, Mitochondria, Mice, Inbred C57BL, Mice, Oligodendroglia, Cellular and Molecular Neuroscience, Spinal Cord, Neurology, Neuroinflammatory Diseases, Animals, Oxidation-Reduction
Abstract

Oligodendrocytes (ODCs) are myelinating cells of the central nervous system (CNS) supporting neuronal survival. Oxidants and mitochondrial dysfunction have been suggested as the main causes of ODC damage during neuroinflammation as observed in multiple sclerosis (MS). Nonetheless, the dynamics of this process remain unclear, thus hindering the design of neuroprotective therapeutic strategies. To decipher the spatio-temporal pattern of oxidative damage and dysfunction of ODC mitochondria in vivo, we created a novel mouse model in which ODCs selectively express the ratiometric H2 O2 biosensor mito-roGFP2-Orp1 allowing for quantification of redox changes in their mitochondria. Using 2-photon imaging of the exposed spinal cord, we observed significant mitochondrial oxidation in ODCs upon induction of the MS model experimental autoimmune encephalomyelitis (EAE). This redox change became already apparent during the preclinical phase of EAE prior to CNS infiltration of inflammatory cells. Upon clinical EAE development, mitochondria oxidation remained detectable and was associated with a significant impairment in organelle density and morphology. These alterations correlated with the proximity of ODCs to inflammatory lesions containing activated microglia/macrophages. During the chronic progression of EAE, ODC mitochondria maintained an altered morphology, but their oxidant levels decreased to levels observed in healthy mice. Taken together, our study implicates oxidative stress in ODC mitochondria as a novel pre-clinical sign of MS-like inflammation and demonstrates that evolving redox and morphological changes in mitochondria accompany ODC dysfunction during neuroinflammation.

Published
2022

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