0000000000241507

AUTHOR

Tamar Mchedlidze

showing 2 related works from this author

Programming of Intestinal Epithelial Differentiation by IL-33 Derived from Pericryptal Fibroblasts in Response to Systemic Infection.

2016

SummaryThe intestinal epithelium constitutes an efficient barrier against the microbial flora. Here, we demonstrate an unexpected function of IL-33 as a regulator of epithelial barrier functions. Mice lacking IL-33 showed decreased Paneth cell numbers and lethal systemic infection in response to Salmonella typhimurium. IL-33 was produced upon microbial challenge by a distinct population of pericryptal fibroblasts neighboring the intestinal stem cell niche. IL-33 programmed the differentiation of epithelial progenitors toward secretory IEC including Paneth and goblet cells. Finally, IL-33 suppressed Notch signaling in epithelial cells and induced expression of transcription factors governing…

0301 basic medicineSalmonella typhimuriumCellular differentiationPopulationNotch signaling pathwayMice TransgenicBiologydigestive systemGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineIntestine SmallmedicineAnimalsHumansCell LineageProgenitor cellIntestinal Mucosaeducationlcsh:QH301-705.5Cell Proliferationeducation.field_of_studySalmonella Infections AnimalReceptors NotchCell growthCell DifferentiationEpithelial CellsFibroblastsInterleukin-33Intestinal epitheliumInterleukin-1 Receptor-Like 1 ProteinCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)Organ SpecificityImmunologyPaneth cellSignal transduction030215 immunologySignal TransductionCell reports
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Interleukin-33-Dependent Innate Lymphoid Cells Mediate Hepatic Fibrosis

2013

SummaryLiver fibrosis is a consequence of chronic liver diseases and thus a major cause of mortality and morbidity. Clinical evidence and animal studies suggest that local tissue homeostasis is disturbed due to immunological responses to chronic hepatocellular stress. Poorly defined stress-associated inflammatory networks are thought to mediate gradual accumulation of extracellular-matrix components, ultimately leading to fibrosis and liver failure. Here we have reported that hepatic expression of interleukin-33 (IL-33) was both required and sufficient for severe hepatic fibrosis in vivo. We have demonstrated that IL-33’s profibrotic effects related to activation and expansion of liver resi…

Liver CirrhosisLiver cytologyImmunologyBiologyLymphocyte ActivationArticle03 medical and health sciencesMice0302 clinical medicineFibrosismedicineHepatic Stellate CellsAnimalsImmunology and AllergyLymphocytesReceptors Interleukin-4 Type IIInterleukin 4Tissue homeostasisCells Cultured030304 developmental biologyCell ProliferationInflammationMice Knockout0303 health sciencesMice Inbred BALB CInterleukin-13InterleukinsInnate lymphoid cellmedicine.diseaseInterleukin-33Adoptive Transfer3. Good healthInterleukin 33Mice Inbred C57BLInfectious DiseasesLiverImmunologyHepatic stellate cellHepatic fibrosisSTAT6 Transcription Factor030215 immunologySignal TransductionImmunity
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