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您的检索式：作者名="Sven G.Meuth"
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| 1 | Blood-brain barrier modeling: challenges and perspectives显示文摘The blood-brain barrier(BBB)forms a highly selective interface between blood and brain.Extensive research efforts have completely changed our view of the BBB in the last years,from a static,impermeable barrier to a dynamic,highly regulated and specific cellular system.The BBB ultrastructurally consists of specialized brain microvascular endothelial cells(BMEC)characterized by low pinocytic activity,absent fenestrations and expression of specific and polarized transcellular transport systems.BMECs are interconnected by protein complexes consisting of tight and adherens junctions leading to high electrical resistance and low paracellular permeability.Attached | Tobias Ruck Stefan Bittner Sven G.Meuth | 2015 | Neural Regeneration Research2015，10，6： | 2 |
| 2 | K_(2P)18.1 translates T cell receptor signals into thymic regulatory T cell development显示文摘It remains largely unclear how thymocytes translate relative differences in T cell receptor(TCR)signal strength into distinct developmental programs that drive the cell fate decisions towards conventional(Tconv)or regulatory T cells(Treg).Following TCR activation,intracellular calcium(Ca^(2+))is the most important second messenger,for which the potassium channel K_(2P)18.1 is a relevant regulator.Here,we identify K_(2P)18.1 as a central translator of the TCR signal into the thymus-derived Treg(tTreg)selection process.TCR signal was coupled to NF-κB-mediated K_(2P)18.1 upregulation in tTreg progenitors.K_(2P)18.1 provided the driving force for sustained Ca^(2+) influx that facilitated NF-κB-and NFAT-dependent expression of FoxP3,the master transcription factor for Treg development and function.Loss of K_(2P)18.1 ion-current function induced a mild lymphoproliferative phenotype in mice,with reduced Treg numbers that led to aggravated experimental autoimmune encephalomyelitis,while a gain-of-function mutation in K_(2P)18.1 resulted in increased Treg numbers in mice.Our findings in human thymus,recent thymic emigrants and multiple sclerosis patients with a dominant-negative missense K_(2P)18.1 variant that is associated with poor clinical outcomes indicate that K_(2P)18.1 also plays a role in human Treg development.Pharmacological modulation of K_(2P)18.1 specifically modulated Treg numbers in vitro and in vivo.Finally,we identified nitroxoline as a K_(2P)18.1 activator that led to rapid and reversible Treg increase in patients with urinary tract infections.Conclusively,our findings reveal how K_(2P)18.1 translates TCR signals into thymic T cell fate decisions and Treg development,and provide a basis for the therapeutic utilization of Treg in several human disorders. | Tobias Ruck Stefanie Bock Steffen Pfeuffer Christina B.Schroeter Derya Cengiz Paul Marciniak Maren Lindner Alexander Herrmann Marie Liebmann Stjepana Kovac Lukas Gola Leoni Rolfes Marc Pawlitzki Nils Opel Tim Hahn Udo Dannlowski Thomas Pap Felix Luessi Julian A.Schreiber Bernhard Wunsch Tanja Kuhlmann Guiscard Seebohm Bjorn Tackenberg Patricia Seja Frank Doring Erhard Wischmeyer Achmet Imam Chasan Johannes Roth Luisa Klotz Gerd Meyer zu Hörste Heinz Wiendl Tobias Marschall Stefan Floess Jochen Huehn Thomas Budde Tobias Bopp Stefan Bittner Sven G.Meuth | 2022 | Cell Research2022，32，1： | 1 |
| 3 | Choroid plexus imaging to track neuroinflammation—a translational model for mouse and human studies显示文摘The choroid plexus(ChP)is a highly vascularized and secretory tissue in each of the brain ventricles that represents the key structure between the blood and the cerebrospinal fluid(CSF).Besides its essential role in CSF production and brain waste clearance pathways,the ChP also contributes to the regulation of central nervous system(CNS)immunosurveillance(Ghersi-Egea et al.,2018).Indeed,the ChP forming the blood-CSF barrier(BCSFB)regulates the entry of immune cells and solute molecules into the brain and vice versa.When antigen-specific,autoreactive immune activation occurs in the periphery,inflammatory cells migrate through the brain barriers towards the CNS(Strominger et al.,2018),initiating neuroinflammatory diseases such as multiple sclerosis(MS). | Muthuraman Muthuraman Mohammadsaleh Oshaghi Vinzenz Fleischer Dumitru Ciolac Ahmed Othman Sven G.Meuth Gabriel Gonzalez-Escamilla Sergiu Groppa | 2023 | Neural Regeneration Research2023，18，3： | 0 |
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