0000000000266902

AUTHOR

Sebastian J. Arnold

0000-0002-2688-9210

showing 3 related works from this author

Tissue microenvironment dictates the fate and tumor-suppressive function of type 3 ILCs

2017

Nussbaum et al. found that tumor suppression through innate lymphoid cells (ILCs) cannot be predicted solely based on the ILC phenotype and lineage but that their immune properties are shaped both by their ontogeny and by the tissue microenvironment they reside in.

0301 basic medicinemedicine.medical_treatmentImmunology314610 Medicine & healthBiology10263 Institute of Experimental ImmunologyArticle31103 medical and health sciencesMiceRAR-related orphan receptor gammaCell Line TumormedicineImmunology and AllergyAnimalsLymphocytesskin and connective tissue diseasesTranscription factorResearch ArticlesMice Knockout2403 ImmunologyInnate lymphoid cellNeoplasms ExperimentalNuclear Receptor Subfamily 1 Group F Member 3PhenotypeCell biologybody regionsKiller Cells NaturalMice Inbred C57BL030104 developmental biologyCytokineCellular MicroenvironmentCell cultureTumor progressionInterleukin 122723 Immunology and AllergyCytokines570 Life sciences; biologyTranscription Factors
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Differentiation of Type 1 ILCs from a Common Progenitor to All Helper-like Innate Lymphoid Cell Lineages

2014

SummaryInnate lymphoid cells (ILCs) are a recently recognized group of lymphocytes that have important functions in protecting epithelial barriers against infections and in maintaining organ homeostasis. ILCs have been categorized into three distinct groups, transcriptional circuitry and effector functions of which strikingly resemble the various T helper cell subsets. Here, we identify a common, Id2-expressing progenitor to all interleukin 7 receptor-expressing, “helper-like” ILC lineages, the CHILP. Interestingly, the CHILP differentiated into ILC2 and ILC3 lineages, but not into conventional natural killer (cNK) cells that have been considered an ILC1 subset. Instead, the CHILP gave rise…

Cellular differentiationLineage (evolution)Bone Marrow CellsGATA3 Transcription FactorBiologyGeneral Biochemistry Genetics and Molecular BiologyMicemedicineAnimalsLymphocytesskin and connective tissue diseasesProgenitorInhibitor of Differentiation Protein 2Receptors Interleukin-7Biochemistry Genetics and Molecular Biology(all)Intracellular parasiteStem CellsInnate lymphoid cellNFIL3Cell DifferentiationT helper cellImmunity InnateMice Inbred C57BLbody regionsmedicine.anatomical_structureImmunologyToxoplasmaIntracellularToxoplasmosisCell
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The Transcription Factor T-bet Is Induced by IL-15 and Thymic Agonist Selection and Controls CD8αα+ Intraepithelial Lymphocyte Development

2014

Summary CD8αα + intraepithelial lymphocytes (IELs) are instrumental in maintaining the epithelial barrier in the intestine. Similar to natural killer cells and other innate lymphoid cells, CD8αα + IELs constitutively express the T-box transcription factor T-bet. However, the precise role of T-bet for the differentiation or function of IELs is unknown. Here we show that mice genetically deficient for T-bet lacked both TCRαβ + and TCRγδ + CD8αα + IELs and thus are more susceptible to chemically induced colitis. Although T-bet was induced in thymic IEL precursors (IELPs) as a result of agonist selection and interleukin-15 (IL-15) receptor signaling, it was dispensable for the generation of IEL…

AgonistCD4-Positive T-Lymphocytesmedicine.drug_classCD8 AntigensReceptors Antigen T-Cell alpha-betaImmunologychemical and pharmacologic phenomenaBiologyCD8-Positive T-Lymphocytesdigestive systemMiceTRANSCRIPTION FACTOR TmedicineTranscriptional regulationImmunology and AllergyAnimalsIntestinal MucosaTranscription factorInterleukin-15Mice KnockoutReceptors Interleukin-15Innate lymphoid cellCell DifferentiationEpithelial CellsReceptors Antigen T-Cell gamma-deltahemic and immune systemsColitisCell biologyIntestinesMice Inbred C57BLInfectious DiseasesInterleukin 15ImmunologyIntraepithelial lymphocyteT-Box Domain ProteinstissuesFunction (biology)Signal TransductionImmunity
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