0000000000021550

AUTHOR

Sandrine Pouly

showing 2 related works from this author

RORgamma-expressing Th17 cells induce murine chronic intestinal inflammation via redundant effects of IL-17A and IL-17F.

2008

Background and Aims IL-17–producing CD4 + T-helper cells (Th17) contribute to chronic autoimmune inflammation in the brain, and levels of Th17-derived cytokines increase in patients with colitis, suggesting a role in pathogenesis. We analyzed the roles of Th17 cells and the transcription factor retinoic acid receptor-related organ receptor (ROR)γ, which regulates Th17 differentiation, in chronic intestinal inflammation. Methods Using an adoptive transfer model of colitis, we compared the colitogenic potential of wild-type, interleukin-17A (IL-17A)–, IL-17F–, IL-22–, and RORγ-deficient CD4 + CD25 − T cells in RAG1-null mice. Results Adoptive transfer of IL-17A–, IL-17F–, or IL-22–deficient T…

Adoptive cell transferNeutrophilsReceptors Retinoic Acidmedicine.medical_treatmentBiologyInflammatory bowel diseasePathogenesisMiceInterferonCell MovementmedicineAnimalsIL-2 receptorColitisCells CulturedReceptors Thyroid HormoneHepatologyInterleukinsInterleukin-17GastroenterologyDendritic CellsT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 3medicine.diseaseColitisAdoptive TransferMice Inbred C57BLCytokineImmunologyChronic Diseasebiology.proteinCytokinesAntibodymedicine.drugGastroenterology
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IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation in mice

2009

The clear association of Th17 cells with autoimmune pathogenicity implicates Th17 cytokines as critical mediators of chronic autoimmune diseases such as EAE. To study the impact of IL-17A on CNS inflammation, we generated transgenic mice in which high levels of expression of IL-17A could be initiated after Cre-mediated recombination. Although ubiquitous overexpression of IL-17A led to skin inflammation and granulocytosis, T cell–specific IL-17A overexpression did not have a perceptible impact on the development and health of the mice. In the context of EAE, neither the T cell–driven overexpression of IL-17A nor its complete loss had a major impact on the development of clinical disease. Sin…

Encephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentT cellEncephalomyelitisPopulation610 Medicine & healthMice TransgenicInflammation2700 General Medicine10263 Institute of Experimental ImmunologyMyelin oligodendrocyte glycoproteinMicemedicineAnimalseducationCells CulturedGlycoproteinseducation.field_of_studybiologybusiness.industryInterleukin-17General MedicineTh1 Cellsmedicine.diseasePeptide FragmentsMice Inbred C57BLCytokinemedicine.anatomical_structureImmunologybiology.protein570 Life sciences; biologyExperimental pathologyFemaleMyelin-Oligodendrocyte GlycoproteinInterleukin 17medicine.symptombusinessGranulocytesResearch Article
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