Search results for "Lymphocyte"

showing 10 items of 2280 documents

Morphological characterization of the blood cells in the endangered Sicilian endemic pond turtle,Emys trinacris(Testudines: Emydidae)

2014

AbstractIn this study, measurements of morphological parameters, sizes and frequencies of peripheral blood cells (erythrocytes, leukocytes, thrombocytes) on blood smear preparation devices stained with May-Grunwald stain were evaluated for both sexes in 20 Emys trinacris (Testudines: Emydidae) specimens. Erythrocytes were higher in male than in female specimens. The leukocyte of E. trinacris contains eosinophil, basophil, monocyte, heterophil and lymphocyte. The eosinophil was higher in males than in females whereas lymphocytes were higher in females than in males. The erythrocyte morphological parameters (EL [erythrocyte length], EW [erythrocyte width], L/W [length/width], ES [erythrocyte …

EmysbiologyEmys orbicularisLymphocyteEndangered speciesTurtle (syntax)Settore BIO/05 - ZoologiaZoologyEmydidaeAnatomyEosinophilbiology.organism_classificationmedicine.anatomical_structureblood smearEmys trinacrisEmys trinacris; blood smear; blood cell morphology; Trachemys scripta elegansmedicineblood cell morphologyAnimal Science and ZoologyEmys trinacriTrachemys scripta elegans
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Apoptosis of oligodendrocytes via Fas and TNF-R1 is a key event in the induction of experimental autoimmune encephalomyelitis.

2005

Abstract In experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, immunization with myelin Ags leads to demyelination and paralysis. To investigate which molecules are crucial for the pathogenesis of EAE, we specifically assessed the roles of the death receptors Fas and TNF-R1. Mice lacking Fas expression in oligodendrocytes (ODCs) were generated and crossed to TNF-R1-deficient mice. To achieve specific deletion of a loxP-flanked fas allele in ODCs, we generated a new insertion transgene, expressing the Cre recombinase specifically in ODCs. Fas inactivation alone as well as the complete absence of TNF-R1 protected mice partially from EAE induced by the imm…

Encephalomyelitis Autoimmune ExperimentalEncephalomyelitisTransgeneT-LymphocytesImmunologyApoptosisMyelin oligodendrocyte glycoproteinMyelinInterferon-gammaMicemedicineImmunology and AllergyAnimalsfas ReceptorReceptorInflammationbiologyMultiple sclerosisExperimental autoimmune encephalomyelitismedicine.diseaseMice Inbred C57BLMyelin-Associated GlycoproteinOligodendrogliamedicine.anatomical_structureApoptosisReceptors Tumor Necrosis Factor Type IImmunologybiology.proteinInterleukin-2Myelin-Oligodendrocyte GlycoproteinMyelin ProteinsDemyelinating DiseasesJournal of immunology (Baltimore, Md. : 1950)
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MAPK3 deficiency drives autoimmunity via DC arming.

2010

DC are professional APC that instruct T cells during the inflammatory course of EAE. We have previously shown that MAPK3 (Erk1) is important for the induction of T-cell anergy. Our goal was to determine the influence of MAPK3 on the capacity of DC to arm T-cell responses in autoimmunity. We report that DC from Mapk3(-/-) mice have a significantly higher membrane expression of CD86 and MHC-II and--when loaded with the myelin oligodendrocyte glycoprotein--show a superior capacity to prime naive T cells towards an inflammatory phenotype than Mapk3(+/+) DC. Nonetheless and as previously described, Mapk3(-/-) mice were only slightly but not significantly more susceptible to myelin oligodendrocyt…

Encephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemOvalbuminImmunologyMedizinAutoimmunityMice TransgenicT-Cell Antigen Receptor SpecificityBiologymedicine.disease_causeAutoimmunityMyelinMiceImmune systemT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsNeuroinflammationGlycoproteinsCD86Mitogen-Activated Protein Kinase 3KinaseHistocompatibility Antigens Class IIDendritic Cellsmedicine.diseaseOligodendrocytePeptide FragmentsSpecific Pathogen-Free OrganismsMice Inbred C57BLmedicine.anatomical_structureRadiation ChimeraImmunologyCytokinesMyelin-Oligodendrocyte GlycoproteinB7-2 AntigenInfiltration (medical)European journal of immunology
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A noninflammatory mRNA vaccine for treatment of experimental autoimmune encephalomyelitis.

2019

Precision therapy for immune tolerance Autoimmune diseases, such as multiple sclerosis (MS), result from a breach of immunological self-tolerance and tissue damage by autoreactive T lymphocytes. Current treatments can cause systemic immune suppression and side effects such as increased risk of infections. Krienke et al. designed a messenger RNA vaccine strategy that lacks adjuvant activity and delivers MS autoantigens into lymphoid dendritic cells. This approach expands a distinct type of antigen-specific effector regulatory T cell that suppresses autoreactivity against targeted autoantigens and promotes bystander suppression of autoreactive T cells against other myelin-specific autoantigen…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisRegulatory T cellEncephalomyelitisAntigen presentationAntigen-Presenting CellsAutoantigensT-Lymphocytes RegulatoryMiceImmune systemAntigenmedicineAnimalsRNA MessengerAntigen-presenting cellImmunosuppression TherapyInflammationVaccines SyntheticMultidisciplinarybusiness.industryEffectorExperimental autoimmune encephalomyelitisBystander Effectmedicine.diseaseMice Inbred C57BLmedicine.anatomical_structureImmunologybusinessPseudouridineScience (New York, N.Y.)
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Myelin-specific T cells also recognize neuronal autoantigen in a transgenic mouse model of multiple sclerosis

2008

T-cell recognition of autoantigens is important in the development of autoimmune disease. Now, Hartmut Wekerle and his colleagues demonstrate that organ-specific autoimmune responses may be driven by T cells that simultaneously respond to two different autoantigens found within the same target tissue. We describe here the paradoxical development of spontaneous experimental autoimmune encephalomyelitis (EAE) in transgenic mice expressing a myelin oligodendrocyte glycoprotein (MOG)-specific T cell antigen receptor (TCR) in the absence of MOG. We report that in Mog-deficient mice (Mog−/−), the autoimmune response by transgenic T cells is redirected to a neuronal cytoskeletal self antigen, neur…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisT-LymphocytesMolecular Sequence DataReceptors Antigen T-CellMice TransgenicCross ReactionsMajor histocompatibility complexAutoantigensGeneral Biochemistry Genetics and Molecular BiologyEpitopeMyelin oligodendrocyte glycoproteinMice03 medical and health sciencesMyelin0302 clinical medicineAntigenNeurofilament ProteinsAnimalsMedicineAmino Acid SequenceMyelin Sheath030304 developmental biologyAutoimmune disease0303 health sciencesbiologybusiness.industryExperimental autoimmune encephalomyelitisT-cell receptorGeneral Medicinemedicine.disease3. Good healthMice Inbred C57BLDisease Models AnimalMyelin-Associated Glycoproteinmedicine.anatomical_structureImmunologybiology.proteinMyelin-Oligodendrocyte GlycoproteinbusinessMyelin Proteins030215 immunologyNature Medicine
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Oligodendrocyte-specific FADD deletion protects mice from autoimmune-mediated demyelination.

2010

Abstract Apoptosis of oligodendrocytes (ODCs), the myelin-producing glial cells in the CNS, plays a central role in demyelinating diseases such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. To investigate the mechanism behind ODC apoptosis in EAE, we made use of conditional knockout mice lacking the adaptor protein FADD specifically in ODCs (FADDODC-KO). FADD mediates apoptosis by coupling death receptors with downstream caspase activation. In line with this, ODCs from FADDODC-KO mice were completely resistant to death receptor-induced apoptosis in vitro. In the EAE model, FADDODC-KO mice followed an ameliorated clinical di…

Encephalomyelitis Autoimmune ExperimentalMultiple Sclerosisgenetic structuresEncephalomyelitisFas-Associated Death Domain ProteinImmunologyApoptosisurologic and male genital diseasesMiceConditional gene knockoutDemyelinating diseasemedicineImmunology and AllergyAnimalsFADDLymphocytesMyelin SheathDeath domainInflammationMice KnockoutbiologyMultiple sclerosisMacrophagesfungiExperimental autoimmune encephalomyelitismedicine.diseaseOligodendrocyteOligodendrogliamedicine.anatomical_structureGene Expression RegulationSpinal CordCancer researchbiology.proteinbiological phenomena cell phenomena and immunityGene DeletionJournal of immunology (Baltimore, Md. : 1950)
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Phosphodiesterase inhibitor pentoxifylline, a selective suppressor of T helper type 1- but not type 2-associated lymphokine production, prevents indu…

1993

The phosphodiesterase inhibitor pentoxifylline (POX), which is known to have pharmacological effects in animal models of multiorgan failure and endotoxin-mediated shock, was tested for its immunosuppressive potential on T lymphocyte activation in vitro and in vivo. POX was found to have a profound inhibitory effect on both mitogen- and antigen-induced proliferation of CD4+ T cells in vitro. This inhibitory activity of the drug could be reproduced by treating T lymphocytes with cAMP analogues during stimulation. Responses of repeatedly in vitro stimulated cells were much more strongly inhibited by the drug and by cAMP analogues than responses of fresh resting lymphocytes. Furthermore, POX co…

Encephalomyelitis Autoimmune ExperimentalPhosphodiesterase InhibitorsEncephalomyelitisT cellImmunologyBiologyLymphocyte ActivationPentoxifyllinemedicineAnimalsImmunology and AllergyPentoxifyllineLymphokinesTumor Necrosis Factor-alphaExperimental autoimmune encephalomyelitisLymphokinevirus diseasesInterleukinT-Lymphocytes Helper-InducerT lymphocytemedicine.diseaseRatsmedicine.anatomical_structureBucladesineRats Inbred LewImmunologyInterleukin-2FemaleTumor necrosis factor alphaInterleukin-4Immunosuppressive Agentsmedicine.drugEuropean Journal of Immunology
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T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma.

2007

T cell functional differentiation is mediated by lineage-specific transcription factors. T helper 17 (Th17) has been recently identified as a distinct Th lineage mediating tissue inflammation. Retinoic acid receptor-related orphan receptor gamma (ROR gamma) was shown to regulate Th17 differentiation; ROR gamma deficiency, however, did not completely abolish Th17 cytokine expression. Here, we report Th17 cells highly expressed another related nuclear receptor, ROR alpha, induced by transforming growth factor-beta and interleukin-6 (IL-6), which is dependent on signal transducer and activator of transcription 3. Overexpression of ROR alpha promoted Th17 differentiation, possibly through the c…

Encephalomyelitis Autoimmune ExperimentalReceptors Retinoic AcidT cellImmunologyRetinoic acidReceptors Cytoplasmic and NuclearElectrophoretic Mobility Shift AssayBiology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineT-Lymphocyte SubsetsmedicineT helper 17 cellImmunology and AllergyAnimalsCell LineageReceptorMOLIMMUNOTranscription factor030304 developmental biologyOrphan receptor0303 health sciencesReceptors Thyroid HormoneReverse Transcriptase Polymerase Chain ReactionInterleukin-17Cell DifferentiationNuclear Receptor Subfamily 1 Group F Member 1T-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3Molecular biologyMice Mutant StrainsCell biologymedicine.anatomical_structureInfectious DiseaseschemistryNuclear receptorSTAT proteinTrans-ActivatorsFemale030215 immunologyImmunity
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Microglial activation milieu controls regulatory T cell responses.

2013

Abstract Although mechanisms leading to brain-specific inflammation and T cell activation have been widely investigated, regulatory mechanisms of local innate immune cells in the brain are only poorly understood. In this study, to our knowledge we show for the first time that MHC class II+CD40dimCD86dimIL-10+ microglia are potent inducers of Ag-specific CD4+Foxp3+ regulatory T cells (Tregs) in vitro. Microglia differentially regulated MHC class II expression, costimulatory molecules, and IL-10 depending on the amount of IFN-γ challenge and Ag dose, promoting either effector T cell or Treg induction. Microglia-induced Tregs were functionally active in vitro by inhibiting Ag-specific prolifer…

Encephalomyelitis Autoimmune ExperimentalRegulatory T cellT cellImmunologychemical and pharmacologic phenomenaMice TransgenicLymphocyte ActivationT-Lymphocytes RegulatoryImmune toleranceInterferon-gammaMiceImmune systemT-Lymphocyte SubsetsmedicineImmune ToleranceImmunology and AllergyAnimalsCells CulturedCD86MHC class IIbiologyMicrogliaHistocompatibility Antigens Class IIFOXP3Brainhemic and immune systemsForkhead Transcription FactorsCoculture TechniquesCell biologyInterleukin-10Mice Inbred C57BLmedicine.anatomical_structureCellular Microenvironmentbiology.proteinMicrogliaJournal of immunology (Baltimore, Md. : 1950)
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Dendritic Cells Ameliorate Autoimmunity in the CNS by Controlling the Homeostasis of PD-1 Receptor+ Regulatory T Cells

2012

SummaryMature dendritic cells (DCs) are established as unrivaled antigen-presenting cells (APCs) in the initiation of immune responses, whereas steady-state DCs induce peripheral T cell tolerance. Using various genetic approaches, we depleted CD11c+ DCs in mice and induced autoimmune CNS inflammation. Unexpectedly, mice lacking DCs developed aggravated disease compared to control mice. Furthermore, when we engineered DCs to present a CNS-associated autoantigen in an induced manner, we found robust tolerance that prevented disease, which coincided with an upregulation of the PD-1 receptor on antigen-specific T cells. Additionally, we showed that PD-1 was necessary for DC-mediated induction o…

Encephalomyelitis Autoimmune ExperimentalT cellProgrammed Cell Death 1 ReceptorImmunologyAntigen presentationCD11cAutoimmunity610 Medicine & healthchemical and pharmacologic phenomenaBiologymedicine.disease_causeAutoantigensT-Lymphocytes RegulatoryB7-H1 AntigenAutoimmunityImmune toleranceMiceImmune systemDownregulation and upregulationImmune TolerancemedicineAnimalsImmunology and AllergyReceptorMice KnockoutAntigen Presentation2403 Immunologyhemic and immune systemsDendritic Cells2725 Infectious DiseasesTh1 CellsCD11c AntigenMice Inbred C57BLInfectious Diseasesmedicine.anatomical_structure10032 Clinic for Oncology and HematologyImmunology2723 Immunology and AllergyTh17 CellsImmunity
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