0000000000309090

AUTHOR

Wolfgang Walter

showing 8 related works from this author

Toxoplasma gondii down-regulates MHC class II gene expression and antigen presentation by murine macrophages via interference with nuclear translocat…

2001

The obligate intracellular protozoan parasite Toxoplasma gondii is able to establish persistent infections within human and animal hosts. We have shown recently that T. gondii down-regulates IFN-γ-induced MHC class II expression in murine bone marrow-derived macrophages (BMMΦ). As shown in this study, the capacity of IFN-γ-activated murine BMMΦ to present ovalbumin to CD4+ T cell hybridomas was dose-dependently inhibited by T. gondii. IFN-γ-induced up-regulation of H2-Aa, H2-Ab, H2-Eb, H2-Ma, H2-Mb, H2-Oa and invariant chain transcripts was prominently down-regulated by T. gondii. Furthermore, mRNA levels of class II transactivator and interferon-regulatory factor-1 were significantly dimin…

MHC class IIbiologyT cellImmunologyAntigen presentationToxoplasma gondiibiology.organism_classificationMolecular biologyMHC Class II Genemedicine.anatomical_structureparasitic diseasesbiology.proteinSTAT proteinmedicineImmunology and AllergySTAT1Signal transductionEuropean Journal of Immunology
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H2-M polymorphism in mice susceptible to collagen-induced arthritis involves the peptide binding groove.

1996

The ability to develop type II collagen (CII)-induced arthritis (CIA) in mice is associated with the major histocompatibilityI-A gene and with as yet poorly defined regulatory molecules of the major histocompatibility complex (MHC) class II antigen processing and presentation pathway. H2-M molecules are thought to be involved in the loading of antigenic peptides into the MHC class II binding cleft. We sequencedH2-Ma, H2-Mb1, andH2-Mb2 genes from CIA-susceptible and-resistant mouse strains and identified four differentMa andMb2 alleles and three differentMb1 alleles defined by polymorphic residues within the predicted peptide binding groove. Most CIA-resistant mouse strains share commonMa, M…

musculoskeletal diseasesImmunologyGenes MHC Class IIMolecular Sequence DataGenes MHC Class IPeptide bindingMice Inbred StrainsMajor histocompatibility complexEpitopeMiceAntigenMHC class IGeneticsAnimalsAmino Acid SequencePhylogenyDNA PrimersMHC class IIPolymorphism GeneticbiologyBase SequenceSequence Homology Amino AcidAntigen processingH-2 AntigensHistocompatibility Antigens Class IIMolecular biologyArthritis ExperimentalHistocompatibilityHaplotypesbiology.proteinCollagenSequence AlignmentImmunogenetics
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Regulation of CD1d expression by murine tumor cells: escape from immunosurveillance or alternate target molecules?

2002

alpha beta+ TCR T cells recognize peptide fragments displayed by MHC-class I or -class II molecules. Recently, additional mechanisms of antigen recognition by T cells have been identified, including CD1-mediated presentation of nonpeptide antigens. Only a limited number of CD1 antigens is retained in the mouse, i.e., the group II CD1 antigens, which are split into CD1D1 and CD1d2. Several T cell subsets have been shown to interact with murine CD1 antigens, including NK cells or "natural T cells" with the invariant V alpha 14 J alpha 281 TCR chain. Even if TAP defects may prevent classical endogenous antigen presentation in tumor cell lines, antigen presentation via CD1 is still functional. …

Cancer ResearchT cellAntigen presentationCD1chemical and pharmacologic phenomenaBiologyNatural killer cellAntigens CD1Immunoenzyme TechniquesInterferon-gammaMiceNK-92Monitoring ImmunologicmedicineCytotoxic T cellAnimalsRNA MessengerAntigen-presenting cellCells CulturedDNA PrimersMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionAntibodies MonoclonalGranulocyte-Macrophage Colony-Stimulating Factorhemic and immune systemsNeoplasms ExperimentalCytotoxicity Tests ImmunologicFlow CytometryCell biologyGene Expression Regulation NeoplasticKiller Cells NaturalMice Inbred C57BLmedicine.anatomical_structureOncologyCD1DImmunologybiology.proteinCytokinesAntigens CD1dInternational journal of cancer
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Differential expression of alternative H2-M isoforms in B cells, dendritic cells and macrophages by proinflammatory cytokines.

1999

Major histocompatibility (MHC) class II heterodimers bind peptides generated by degradation of endocytosed antigens and display them on the surface of antigen presenting cells (APCs) for recognition by CD4+ T cells. Efficient loading of MHC class II molecules with peptides is catalyzed by the MHC class II-like molecule H2-M. The coordinate regulation of MHC class II and H2-M expression is a prerequisite for efficient MHC class II/peptide assembly in APCs determining both the generation of the T cell repertoire in the thymus and cellular immune responses in the periphery. Here we show that expression of H2-M and MHC class II genes is coordinately and cell type-specific regulated in splenic B…

CD74ImmunologyAntigen presentationGenes MHC Class IICD1Antigen-Presenting CellsGene ExpressionIn Vitro TechniquesMHC Class II GeneMiceMHC class IAnimalsProtein IsoformsMolecular BiologyDNA PrimersMHC class IIB-LymphocytesHLA-D AntigensMice Inbred BALB CbiologyBase SequenceAntigen processingHistocompatibility Antigens Class IIDendritic CellsMHC restrictionMolecular biologybiology.proteinMacrophages PeritonealCytokinesInflammation MediatorsMolecular immunology
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H2-M, a facilitator of MHC class II peptide loading, and its negative modulator H2-O are differentially expressed in response to proinflammatory cyto…

2000

H2-M is a major histocompatibility complex (MHC) class II-like molecule that catalyzes peptide binding to MHC class II molecules. Recently, the H2-O heterodimer, encoded by H2-Oa and H2-Ob in the MHC class II region, has been shown to be physically associated with H2-M in B cells and to downregulate H2-M function. Examination of H2-O expression in freshly isolated mouse organs revealed that H2-Oa- and H2-Ob-specific transcripts are present in both lymphoid and nonlymphoid tissues. To evaluate the gene regulation and functional impact of H2-O on antigen presentation, we examined the effects on MHCII, invariant chain (Ii), H2-M, and H2-O gene expression of interleukin (IL)-4, IL-10, and inter…

CD74ImmunologyAntigen presentationchemical and pharmacologic phenomenaMajor histocompatibility complexInterferon-gammaMiceMHC class IGeneticsCIITAAnimalsTissue DistributionRNA MessengerAntigen PresentationHLA-D AntigensMHC class IIbiologyAntigen processingHistocompatibility Antigens Class IINuclear ProteinsMHC restrictionMolecular biologyInterleukin-10Antigens Differentiation B-LymphocyteGene Expression RegulationMice Inbred DBATrans-Activatorsbiology.proteinInterleukin-4PeptidesImmunogenetics
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Interleukin-7 or Interleukin-15 Enhances Survival ofMycobacterium tuberculosis-Infected Mice

2000

ABSTRACTBoth antigen-presenting cells and immune effector cells are required to effectively eradicate or containMycobacterium tuberculosis-infected cells. A variety of cytokines are involved to ensure productive “cross talk” between macrophages and T lymphocytes. For instance, infection of macrophages with mycobacteria leads to effective interleukin-7 (IL-7) and IL-15 secretion, and both cytokines are able to maintain strong cellular immune responses of α/β and γ/δ T cells. Here we show that either cytokine is able to enhance survival ofM. tuberculosis-infected BALB/c mice significantly compared to application of IL-2, IL-4, or phosphate-buffered saline (as a control). Enhanced survival cou…

Adoptive cell transfermedicine.medical_treatmentImmunologySpleenBiologyMicrobiologyMiceImmune systemmedicineAnimalsTuberculosisInterleukin-15Mice Inbred BALB CInterleukin-7InterleukinMycobacterium tuberculosisT lymphocyteAdoptive TransferDisease Models AnimalInfectious Diseasesmedicine.anatomical_structureCytokineInterleukin 15Microbial Immunity and VaccinesImmunologyCytokinesFemaleParasitologyTumor necrosis factor alphaSpleenInfection and Immunity
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H2-Mβ1 and H2-Mβ2 Heterodimers Equally Promote CLIP Removal in I-Aq Molecules from Autoimmune-prone DBA/1 Mice

2001

Antigen-presenting cells degrade endocytosed antigens, e.g. collagen type II, into peptides that are bound and presented to arthritogenic CD4(+) helper T cells by major histocompatibility complex (MHC) class II molecules. Efficient loading of many MHC class II alleles with peptides requires the assistance of H2-M (HLA-DM in humans), a heterodimeric MHC class II-like molecule that facilitates CLIP removal from MHC class II molecules and aids to shape the peptide repertoire presented by MHC class II to CD4(+) T cells. In contrast to the HLA-DM region in humans, the beta-chain locus is duplicated in mice, with the H2-Mb1 beta-chain distal to H2-Mb2 and the H2-Ma alpha-chain gene. H2-M alleles …

Gene isoformAntigen PresentationMHC class IICD74ArthritisHistocompatibility Antigens Class IICD1AutoimmunityCell BiologyMHC restrictionBiologyMajor histocompatibility complexBiochemistryMolecular biologyCell LineAntigens Differentiation B-LymphocyteMiceAntigenMice Inbred DBAMHC class Ibiology.proteinAnimalsHumansGenetic Predisposition to DiseaseMolecular BiologyJournal of Biological Chemistry
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Differential expression of the murine mannose-binding lectins A and C in lymphoid and nonlymphoid organs and tissues.

2003

Abstract Mannose-binding lectin (MBL), a member of the collectin family, binds to carbohydrate structures on the surfaces of micro-organisms and may serve as a recognition molecule of the lectin pathway of complement activation. In rodents two forms, MBL-A and MBL-C, were described and shown to be products of two related, but uncoupled, genes. The liver is the main source of MBL biosynthesis. For rat MBL-A, expression has also been described in the kidney. Here we report that the two forms of murine MBL are differentially expressed in a number of nonhepatic tissues. Real-time RT-PCR revealed that the liver is the major site of expression for both MBL genes. Lower copy numbers were found in …

MaleLymphoid TissueImmunologyCollectinchemical and pharmacologic phenomenaIn situ hybridizationMannose-Binding LectinMiceIntestine SmallImmunology and AllergyAnimalsProtein IsoformsIn Situ HybridizationMannan-binding lectinMice Inbred BALB CInnate immune systembiologyLectinbacterial infections and mycosesAcquired immune systemMolecular biologyImmunohistochemistryComplement systemAnimals NewbornLiverOrgan SpecificityLectin pathwaybiology.proteinFemaleSpleenJournal of immunology (Baltimore, Md. : 1950)
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