Search results for "Immunology and Inflammation"

showing 5 items of 5 documents

Notch and TLR signaling coordinate monocyte cell fate and inflammation

2020

AbstractConventional Ly6Chi monocytes have developmental plasticity for a spectrum of differentiated phagocytes. Here we show, using conditional deletion strategies in a mouse model of Toll-like receptor (TLR) 7-induced inflammation, that the spectrum of developmental cell fates of Ly6Chi monocytes, and the resultant inflammation, is coordinately regulated by TLR and Notch signaling. Cell-intrinsic Notch2 and TLR7-Myd88 pathways independently and synergistically promote Ly6Clo patrolling monocyte development from Ly6Chi monocytes under inflammatory conditions, while impairment in either signaling axis impairs Ly6Clo monocyte development. At the same time, TLR7 stimulation in the absence of …

0301 basic medicineMouseQH301-705.5ScienceNotch signaling pathwayInflammationSpleenBiologyCell fate determinationSystemic inflammationGeneral Biochemistry Genetics and Molecular BiologyMonocytesimmunology03 medical and health sciencesMice0302 clinical medicineImmunology and InflammationmedicineAnimalsReceptor Notch2Biology (General)Receptormousemacrophage differentiationInflammationMembrane GlycoproteinsGeneral Immunology and MicrobiologyGeneral NeuroscienceMonocyteQRCell DifferentiationTLR signalingGeneral MedicineTLR7notch signalingCell biology030104 developmental biologymedicine.anatomical_structureToll-Like Receptor 7inflammationmonocytes and macrophagesMedicinemedicine.symptom030215 immunologySignal TransductionResearch Article
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Distinct single-component adjuvants steer human DC-mediated T-cell polarization via Toll-like receptor signaling toward a potent antiviral immune res…

2021

Significance Vaccines profit from the addition of adjuvants to better and more specifically initiate, amplify, and shape immune responses. Although the number of adjuvant candidates has steadily increased, peaking in the current SARS-CoV-2 pandemic, little is known about their inherent mode of action. Using human blood immune cells, we established a multilayer method to systematically assess the adjuvants’ effects on innate and adaptive immune cells. By employing a multiplex analysis with cells from 30 different donors, we determined important patterns of adjuvant function. Moreover, we demonstrate correlates of an antiviral immune response using a Toll-like receptor 7/8 ligand adjuvant and…

AdultMaleAdolescentT-LymphocytesMonophosphoryl Lipid ALipid Achemistry.chemical_compoundImmunology and InflammationImmune systemAdjuvants ImmunologicInterferonTLRmedicineHumansprimary human cellsAgedImmunity CellularToll-like receptorMultidisciplinarySARS-CoV-2ChemistryToll-Like ReceptorsImidazolesCOVID-19Dendritic CellsTLR7biochemical phenomena metabolism and nutritionBiological SciencesMiddle AgedCOVID-19 ; TLR ; primary human cells ; adjuvants ; mRNA vaccines420Cell biologymRNA vaccinesLipid AadjuvantsTLR4[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleResiquimodmedicine.drugProceedings of the National Academy of Sciences
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Intrinsic TNFR2 signaling in T regulatory cells provides protection in CNS autoimmunity

2018

Significance In spite of TNF involvement in the pathogenesis of multiple sclerosis (MS), systemic TNF neutralization in MS patients was not successful. One of the possible reasons is that TNF possesses both pathogenic and protective features that may be related to TNFR1 versus TNFR2 receptor engagement. This study uncovers one of such protective functions of TNF mediated by intrinsic TNFR2 signaling in Treg cells. In mice bearing humanized TNF and TNFR2 genetic loci, TNFR2 ablation restricted to Treg cells led to reduced capacity to control Th17 cell responses, exacerbated experimental autoimmune encephalomyelitis (EAE) development, and affected the maintenance of Treg cells. These findings…

Central Nervous System0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT regulatory cellsmedicine.medical_treatmentAutoimmunitychemical and pharmacologic phenomenaBiologymedicine.disease_causeT-Lymphocytes RegulatoryneuroinflammationAutoimmunityMice03 medical and health sciencesImmunology and Inflammation0302 clinical medicineImmune systemmedicineAnimalsHumansReceptors Tumor Necrosis Factor Type IIIL-2 receptorCells CulturedNeuroinflammationMice KnockoutAutoimmune diseaseMultidisciplinaryEAETumor Necrosis Factor-alphaExperimental autoimmune encephalomyelitisFOXP3hemic and immune systemsBiological Sciencesmedicine.diseaseTNF/TNFR2Mice Inbred C57BLDisease Models Animalhumanized mice030104 developmental biologyCytokineGene Expression RegulationImmunology030215 immunologyProceedings of the National Academy of Sciences
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Unraveling the T-B tangle in anti-CD20 multiple sclerosis therapy.

2019

Significance Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system. CD8+ T cells have been strongly implicated in MS pathogenesis, but it is unclear whether myelin is a CD8+ T cell autoantigenic target in MS. This study demonstrated that while myelin-specific CD8+ T cells are present at similar frequencies in untreated MS patients and healthy subjects, the proportion of memory and CD20-expressing myelin-specific CD8+ T cells was increased in MS patients, suggesting prior antigen encounter. This activated phenotype was reversible as the memory and CD20-expressing populations of certain myelin-specific CD8+ T cells were reduced following anti-CD20 trea…

Multiple SclerosisCentral nervous systemAxonal lossDiseaseCD8-Positive T-LymphocytesCD8+ T cellsanti-CD20 therapy03 medical and health sciences0302 clinical medicineImmune systemImmunology and InflammationAntigenmedicineHumansMyelin SheathMultidisciplinarybusiness.industryMultiple sclerosisExperimental autoimmune encephalomyelitisBiological Sciencesmedicine.diseaseAntigens CD20medicine.anatomical_structureImmunizationImmunologybusinessmyelin antigen030217 neurology & neurosurgery030215 immunologyProceedings of the National Academy of Sciences of the United States of America
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Pro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation.

2021

Significance Multiple sclerosis (MS) is a neuroinflammatory, demyelinating disease that represents one of the most frequent causes of irreversible disability in young adults. Treatment options to halt disability are limited. We discovered that T helper (Th)17 cells in contact with oligodendrocytes produce higher levels of glutamate and induce significantly greater oligodendrocyte damage than their Th2 counterpart. Blockade of CD29, which is linked to glutamate release pathways and expressed in high levels on Th17 cells, preserved human oligodendrocyte processes from Th17-mediated injury. Our data thus provide evidence for the direct and deleterious attack of Th17 cells on the myelin compart…

Programmed cell deathEncephalomyelitis Autoimmune ExperimentalCentral nervous systemFreund's AdjuvantoligodendrocytesMice Transgenicglutamate03 medical and health sciencesMyelinMice0302 clinical medicineImmunology and Inflammationintravital microscopymedicineAnimalsNeuroinflammation030304 developmental biologyInflammationMice Knockout0303 health sciencesMultidisciplinaryChemistryMultiple sclerosisGlutamate receptorMembrane ProteinsCD29Biological SciencesCD29 blockademedicine.disease420Oligodendrocyte3. Good healthCell biologyDNA-Binding ProteinsMice Inbred C57BLOligodendrogliamedicine.anatomical_structurePertussis ToxinTh17 CellsMyelin-Oligodendrocyte Glycoprotein030217 neurology & neurosurgeryProceedings of the National Academy of Sciences of the United States of America
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