0000000000243727

AUTHOR

Anne Müller

showing 4 related works from this author

Keratinocyte-derived IκBζ drives psoriasis and associated systemic inflammation.

2019

The transcriptional activator IκBζ is a key regulator of psoriasis, but which cells mediate its pathogenic effect remains unknown. Here we found that IκBζ expression in keratinocytes triggers not only skin lesions but also systemic inflammation in mouse psoriasis models. Specific depletion of IκBζ in keratinocytes was sufficient to suppress the induction of imiquimod- or IL-36–mediated psoriasis. Moreover, IκBζ ablation in keratinocytes prevented the onset of psoriatic lesions and systemic inflammation in keratinocyte-specific IL-17A–transgenic mice. Mechanistically, this psoriasis protection was mediated by IκBζ deficiency in keratinocytes abrogating the induction of specific proinflammato…

0301 basic medicineKeratinocytesMaleAutoimmune diseasesInflammationMice TransgenicAutoimmunityDermatologySystemic inflammationmedicine.disease_causeAutoimmunityProinflammatory cytokine03 medical and health sciencesMice0302 clinical medicinePsoriasismedicineAnimalsPsoriasisCells CulturedAdaptor Proteins Signal TransducingSkinInflammationInnate immunityInnate immune systembusiness.industryInterleukin-17General Medicinemedicine.diseaseCXCL2030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchFemalemedicine.symptomKeratinocytebusinessResearch ArticleJCI insight
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Helicobacter pylori gamma-glutamyl transpeptidase and vacuolating cytotoxin promote gastric persistence and immune tolerance

2013

Infection with the gastric bacterial pathogen Helicobacter pylori is typically contracted in early childhood and often persists for decades. The immunomodulatory properties of H. pylori that allow it to colonize humans persistently are believed to also account for H. pylori ’s protective effects against allergic and chronic inflammatory diseases. H. pylori infection efficiently reprograms dendritic cells (DCs) toward a tolerogenic phenotype and induces regulatory T cells (Tregs) with highly suppressive activity in models of allergen-induced asthma. We show here that two H. pylori virulence determinants, the γ-glutamyl transpeptidase GGT and the vacuolating cytotoxin VacA, contribute critic…

TransgeneVirulenceMice Transgenicbacterial virulence factorspersistence strategieshygiene hypothesisMicrobiologyImmune toleranceMice03 medical and health sciences0302 clinical medicineBacterial ProteinsIn vivoImmune ToleranceAnimalsGamma-glutamyltransferasehuman microbiotaPathogen030304 developmental biology0303 health sciences1000 MultidisciplinaryMultidisciplinaryHelicobacter pyloribiologyStomach10061 Institute of Molecular Cancer Researchgamma-GlutamyltransferaseBiological SciencesHelicobacter pyloribiology.organism_classificationbacterial infections and mycosesCoculture TechniquesIn vitrodigestive system diseases3. Good healthMice Inbred C57BLImmunologybiology.protein570 Life sciences; biology030211 gastroenterology & hepatologypersistent bacterial infection
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Host glycoprotein Gp96 and scavenger receptor SREC interact with PorB of disseminating Neisseria gonorrhoeae in an epithelial invasion pathway.

2007

Neisseria gonorrhoeae expresses numerous surface proteins that mediate bacterial adherence and invasion during infection. Gonococci expressing serotype A of the major outer membrane porin PorB (PorB(IA)) are frequently isolated from patients with severe disseminating infections. PorB(IA) triggers efficient adherence and invasion under low phosphate conditions mimicking systemic bloodstream infections. Here, we identify the human heat shock glycoprotein Gp96 and the scavenger receptor SREC as PorB(IA)-specific receptors. Gonococci expressing PorB(IA), but not those expressing PorB serotype B instead, bind to purified native or recombinant Gp96. Depletion of Gp96 from host cells prevented adh…

SerotypeCancer ResearchMICROBIO2405 ParasitologyPorinsBiologymedicine.disease_causeEndoplasmic ReticulumMicrobiologyBacterial Adhesionlaw.inventionMicrobiologyGonorrhealawVirologyImmunology and Microbiology(all)medicineAnimalsHumansScavenger receptorReceptorMolecular BiologyCells Culturedchemistry.chemical_classificationMembrane Glycoproteins10061 Institute of Molecular Cancer Research2404 MicrobiologyEpithelial CellsNeisseria gonorrhoeaeScavenger Receptors Class FchemistryPorin2406 VirologyRecombinant DNANeisseria gonorrhoeae570 Life sciences; biologyParasitologyGlycoproteinBacterial outer membraneProtein BindingCell hostmicrobe
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Effective treatment of allergic airway inflammation with Helicobacter pylori immunomodulators requires BATF3-dependent dendritic cells and IL-10

2014

The prevalence of allergic asthma and other atopic diseases has reached epidemic proportions in large parts of the developed world. The gradual loss of the human indigenous microbiota has been held responsible for this trend. The bacterial pathogen Helicobacter pylori is a constituent of the normal gastric microbiota whose presence has been inversely linked to allergy and asthma in humans and experimental models. Here we show that oral or i.p. tolerization with H. pylori extract prevents the airway hyperresponsiveness, bronchoalveolar eosinophilia, pulmonary inflammation, and Th2 cytokine production that are hallmarks of allergen-induced asthma in mice. Asthma protection is not conferred by…

Allergybacterial persistence determinantsT-Lymphocytes Regulatorybacterial immunomodulationImmune toleranceMiceBacterial ProteinsImmune TolerancemedicineAnimalsHumansImmunologic FactorsEosinophiliaAsthmaMice KnockoutAntigens Bacterial1000 MultidisciplinaryMultidisciplinaryHelicobacter pyloribiologyallergy and asthma prevention10061 Institute of Molecular Cancer ResearchInterleukin-18tolerogenic dendritic cellsDendritic Cellsgamma-GlutamyltransferaseDendritic cellBiological SciencesAllergensHelicobacter pyloribacterial infections and mycosesmedicine.diseasebiology.organism_classificationAsthmaInterleukin-10respiratory tract diseases3. Good healthMice Inbred C57BLRepressor ProteinsDisease Models AnimalInterleukin 10Basic-Leucine Zipper Transcription FactorsImmunology570 Life sciences; biologyInterleukin 18medicine.symptom
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