0000000000505573

AUTHOR

Vera Schwierzeck

showing 3 related works from this author

A T-bet gradient controls the fate and function of CCR6−RORγt+ innate lymphoid cells

2013

At mucosal surfaces, the immune system should not initiate inflammatory immune responses to the plethora of antigens constantly present in the environment, but should remain poised to unleash a potent assault on intestinal pathogens. The transcriptional programs and regulatory factors required for immune cells to switch from homeostatic (often tissue-protective) function to potent antimicrobial immunity are poorly defined. Mucosal retinoic-acid-receptor-related orphan receptor-γt-positive (RORγt(+)) innate lymphoid cells (ILCs) are emerging as an important innate lymphocyte population required for immunity to intestinal infections. Various subsets of RORγt(+) ILCs have been described but th…

education.field_of_studyMultidisciplinaryLymphocyteCellular differentiationInnate lymphoid cellPopulationhemic and immune systemschemical and pharmacologic phenomenaC-C chemokine receptor type 6Biologymedicine.anatomical_structureImmune systemImmunityRAR-related orphan receptor gammaImmunologymedicineskin and connective tissue diseaseseducationNature
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Interferon-λ and interleukin 22 act synergistically for the induction of interferon-stimulated genes and control of rotavirus infection.

2015

The epithelium is the main entry point for many viruses, but the processes that protect barrier surfaces against viral infections are incompletely understood. Here we identified interleukin 22 (IL-22) produced by innate lymphoid cell group 3 (ILC3) as an amplifier of signaling via interferon-λ (IFN-λ), a synergism needed to curtail the replication of rotavirus, the leading cause of childhood gastroenteritis. Cooperation between the receptor for IL-22 and the receptor for IFN-λ, both of which were 'preferentially' expressed by intestinal epithelial cells (IECs), was required for optimal activation of the transcription factor STAT1 and expression of interferon-stimulated genes (ISGs). These d…

ImmunologyImmunoblottingMolecular Sequence DataGene ExpressionMice Transgenicmedicine.disease_causeRotavirus InfectionsCell LineMadin Darby Canine Kidney CellsInterleukin 22DogsInterferonRotavirusChlorocebus aethiopsmedicineImmunology and AllergyAnimalsHumansSTAT1Intestinal MucosaReceptors CytokineVero CellsMice KnockoutbiologyReverse Transcriptase Polymerase Chain ReactionInterleukinsInnate lymphoid cellInterleukinDrug SynergismEpithelial CellsVirology3. Good healthIntestinesMice Inbred C57BLSTAT1 Transcription FactorViral replicationImmunologybiology.proteinVero cellCytokinesCaco-2 CellsHT29 Cellsmedicine.drugNature immunology
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Host microbiota constantly control maturation and function of microglia in the CNS.

2015

As the tissue macrophages of the CNS, microglia are critically involved in diseases of the CNS. However, it remains unknown what controls their maturation and activation under homeostatic conditions. We observed substantial contributions of the host microbiota to microglia homeostasis, as germ-free (GF) mice displayed global defects in microglia with altered cell proportions and an immature phenotype, leading to impaired innate immune responses. Temporal eradication of host microbiota severely changed microglia properties. Limited microbiota complexity also resulted in defective microglia. In contrast, recolonization with a complex microbiota partially restored microglia features. We determ…

Central Nervous SystemMaleCellGut–brain axis610 Medicine & healthBiologydigestive systemReceptors G-Protein-CoupledMiceImmunitymedicineAnimalsHomeostasis10239 Institute of Laboratory Animal ScienceReceptorInnate immune systemMicrogliaGeneral NeuroscienceMicrobiota2800 General NeuroscienceFatty Acids VolatilePhenotypeImmunity InnateMice Inbred C57BLmedicine.anatomical_structurenervous systemImmunology570 Life sciences; biology590 Animals (Zoology)FemaleMicrogliaNeuroscienceHomeostasisNature neuroscience
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