0000000000883774

AUTHOR

Michael K. Schuhmann

showing 2 related works from this author

Fingolimod (FTY720-P) Does Not Stabilize the Blood–Brain Barrier under Inflammatory Conditions in an in Vitro Model

2015

Breakdown of the blood-brain barrier (BBB) is an early hallmark of multiple sclerosis (MS), a progressive inflammatory disease of the central nervous system. Cell adhesion in the BBB is modulated by sphingosine-1-phosphate (S1P), a signaling protein, via S1P receptors (S1P\(_1\)). Fingolimod phosphate (FTY720-P) a functional S1P\(_1\) antagonist has been shown to improve the relapse rate in relapsing-remitting MS by preventing the egress of lymphocytes from lymph nodes. However, its role in modulating BBB permeabilityin particular, on the tight junction proteins occludin, claudin 5 and ZO-1has not been well elucidated to date. In the present study, FTY720-P did not change the transendotheli…

Pathologytight junctionsDrug Evaluation PreclinicalApoptosisVascular permeabilityOccludinlcsh:ChemistryMedicinelcsh:QH301-705.5Cells CulturedSpectroscopyTight junctionrat brain microvascular endothelial cell cultureGeneral MedicineFingolimodComputer Science ApplicationsCell biologyEndothelial stem cellmedicine.anatomical_structureMatrix Metalloproteinase 2Immunosuppressive AgentsFTY720-P; blood-brain barrier; rat brain microvascular endothelial cell culture; inflammation; tight junctionsmedicine.drugmedicine.medical_specialtyMultiple SclerosisMAP Kinase Signaling SystemBlood–brain barrierArticleCatalysisCapillary PermeabilityInorganic ChemistryOccludinFingolimod HydrochlorideAnimalsFTY720-Pddc:610Physical and Theoretical ChemistryClaudinMolecular BiologyFingolimod Hydrochloridebusiness.industryOrganic ChemistryEndothelial Cellsblood-brain barrierRatslcsh:Biology (General)lcsh:QD1-999inflammationMicrovesselsbusinessInternational Journal of Molecular Sciences
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Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells

2016

Aberrant immune responses represent the underlying cause of central nervous system (CNS) autoimmunity, including multiple sclerosis (MS). Recent evidence implicated the crosstalk between coagulation and immunity in CNS autoimmunity. Here we identify coagulation factor XII (FXII), the initiator of the intrinsic coagulation cascade and the kallikrein–kinin system, as a specific immune cell modulator. High levels of FXII activity are present in the plasma of MS patients during relapse. Deficiency or pharmacologic blockade of FXII renders mice less susceptible to experimental autoimmune encephalomyelitis (a model of MS) and is accompanied by reduced numbers of interleukin-17A-producing T cells.…

AdultMale0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple Sclerosisanimal structuresT-LymphocytesScienceMedizinGeneral Physics and AstronomyKininsCoagulation Factor XIIAdaptive ImmunityBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyReceptors Urokinase Plasminogen ActivatorAutoimmunityYoung Adult03 medical and health sciencesImmune systemddc:570medicineAnimalsHumansddc:610cardiovascular diseasesNeuroinflammationAgedFactor XIIMultidisciplinaryInterleukin-17QExperimental autoimmune encephalomyelitisCell DifferentiationDendritic CellsGeneral ChemistryMiddle Agedmedicine.diseaseAcquired immune systemMice Inbred C57BL030104 developmental biologyNeuroimmunologyFactor XIIImmunologyFemaleKallikreinscirculatory and respiratory physiologyNature Communications
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