0000000000017368

AUTHOR

Carsten Schelmbauer

showing 2 related works from this author

Cutting Edge: IL-6–Driven Immune Dysregulation Is Strictly Dependent on IL-6R α-Chain Expression

2020

Abstract IL-6 binds to the IL-6R α-chain (IL-6Rα) and signals via the signal transducer gp130. Recently, IL-6 was found to also bind to the cell surface glycoprotein CD5, which would then engage gp130 in the absence of IL-6Rα. However, the biological relevance of this alternative pathway is under debate. In this study, we developed a mouse model, in which murine IL-6 is overexpressed in a CD11c-Cre–dependent manner. Transgenic mice developed a lethal immune dysregulation syndrome with increased numbers of Ly-6G+ neutrophils and Ly-6Chi monocytes/macrophages. IL-6 overexpression promoted activation of CD4+ T cells while suppressing CD5+ B-1a cell development. However, additional ablation of …

Genetically modified mouseImmunologyInflammationMice Transgenicmedicine.disease_cause03 medical and health sciencesMice0302 clinical medicineRare DiseasesmedicineImmunology and AllergyAnimals2.1 Biological and endogenous factorsInflammatory and Immune SystemReceptorSTAT3biologyCell growthChemistryInterleukin-6Immune dysregulationGlycoprotein 130Receptors Interleukin-6Cell biologybiology.proteinAlternative complement pathwaymedicine.symptom030215 immunologySignal TransductionThe Journal of Immunology
researchProduct

IL ‐1 signaling is critical for expansion but not generation of autoreactive GM ‐ CSF + Th17 cells

2016

Abstract Interleukin‐1 (IL‐1) is implicated in numerous pathologies, including multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the exact mechanism by which IL‐1 is involved in the generation of pathogenic T cells and in disease development remains largely unknown. We found that following EAE induction, pertussis toxin administration leads to IL‐1 receptor type 1 (IL‐1R1)‐dependent IL‐1β expression by myeloid cells in the draining lymph nodes. This myeloid‐derived IL‐1β did not vitally contribute to the generation and plasticity of Th17 cells, but rather promoted the expansion of a GM‐CSF + Th17 cell subset, thereby enhancing its encephalitog…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalBiologymedicine.disease_causePertussis toxinGeneral Biochemistry Genetics and Molecular BiologyAutoimmunityMice03 medical and health sciences0302 clinical medicineMediatormedicineAnimalsInducerMolecular BiologyCell ProliferationGeneral Immunology and MicrobiologyGeneral NeuroscienceMultiple sclerosisExperimental autoimmune encephalomyelitisGranulocyte-Macrophage Colony-Stimulating FactorArticlesmedicine.diseaseCell biology030104 developmental biologyPertussis ToxinT cell subsetImmunologyTh17 CellsLymphInterleukin-1030215 immunologyThe EMBO Journal
researchProduct