0000000000968199

AUTHOR

Friederike Kruse

showing 2 related works from this author

Targeting cellular fatty acid synthesis limits T helper and innate lymphoid cell function during intestinal inflammation and infection

2019

CD4+ T cells contribute critically to a protective immune response during intestinal infections, but have also been implicated in the aggravation of intestinal inflammatory pathology. Previous studies suggested that T helper type (Th)1 and Th17 cells depend on de novo fatty acid (FA) synthesis for their development and effector function. Here, we report that T-cell-specific targeting of the enzyme acetyl-CoA carboxylase 1 (ACC1), a major checkpoint controlling FA synthesis, impaired intestinal Th1 and Th17 responses by limiting CD4+ T-cell expansion and infiltration into the lamina propria in murine models of colitis and infection-associated intestinal inflammation. Importantly, pharmacolog…

0301 basic medicineImmunologyBiologyMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemRAR-related orphan receptor gammamedicineAnimalsImmunology and AllergyFatty acid synthesisBarrier functionLamina propriaEffectorFatty AcidsInnate lymphoid cellT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3ColitisInflammatory Bowel DiseasesImmunity InnateBiosynthetic PathwaysDisease Models Animal030104 developmental biologymedicine.anatomical_structurechemistryImmunologyLipogenesisBiomarkersAcetyl-CoA Carboxylase030215 immunologyMucosal Immunology
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Epithelium‐specific MyD88 signaling, but not DCs or macrophages, control acute intestinal infection with Clostridium difficile

2019

Infection with Clostridium difficile is one of the major causes of health care acquired diarrhea and colitis. Signaling though MyD88 downstream of TLRs is critical for initiating the early protective host response in mouse models of C. difficile infection (CDI). In the intestine, MyD88 is expressed in various tissues and cell types, such as the intestinal epithelium and mononuclear phagocytes (MNP), including DC or macrophages. Using a genetic gain-of-function system, we demonstrate here that restricting functional MyD88 signaling to the intestinal epithelium, but also to MNPs is sufficient to protect mice during acute CDI by upregulation of the intestinal barrier function and recruitment o…

0301 basic medicineCell typeImmunologyBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationmedicineAnimalsImmunology and AllergyIntestinal MucosaColitisEnterocolitis PseudomembranousBarrier functionClostridioides difficileMacrophagesDendritic CellsClostridium difficilemedicine.diseaseIntestinal epitheliumPhenotypeEpitheliumDisease Models Animal030104 developmental biologymedicine.anatomical_structureHost-Pathogen InteractionsMyeloid Differentiation Factor 88ImmunologySignal Transduction030215 immunologyEuropean Journal of Immunology
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