2025
Heterogeneity of IL-15-expressing mesenchymal stromal cells controls natural killer cell development and immune cell homeostasis
Stecher C, Bischl R, Schmid-Böse A, Ferstl S, Potzmann E, Frank M, Braun N, Farlik M, Flavell R, Herndler-Brandstetter D. Heterogeneity of IL-15-expressing mesenchymal stromal cells controls natural killer cell development and immune cell homeostasis. Nature Communications 2025, 16: 5949. PMID: 40595636, PMCID: PMC12218584, DOI: 10.1038/s41467-025-61231-0.Peer-Reviewed Original ResearchConceptsMemory CD8+ T cellsCD8+ T cellsMature NK cellsMesenchymal stromal cellsImmune cell lineagesBone marrowNK cellsT cellsStromal cellsNatural killerBone marrows of old miceBM mesenchymal stromal cellsNatural killer cell developmentCell lineagesHematopoietic stem cellsDeletion mouse modelIL-15 expressionImmune cell homeostasisNKT cellsIL-15Old miceMouse modelConditional deletionMicroenvironmental nicheStem cells
2023
Nogo receptor-Fc delivered by haematopoietic cells enhances neurorepair in a multiple sclerosis model
Ye S, Theotokis P, Lee J, Kim M, Nheu D, Ellen O, Bedford T, Ramanujam P, Wright D, McDonald S, Alrehaili A, Bakhuraysah M, Kang J, Siatskas C, Tremblay C, Curtis D, Grigoriadis N, Monif M, Strittmatter S, Petratos S. Nogo receptor-Fc delivered by haematopoietic cells enhances neurorepair in a multiple sclerosis model. Brain Communications 2023, 5: fcad108. PMID: 37091588, PMCID: PMC10116608, DOI: 10.1093/braincomms/fcad108.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisAutoimmune encephalomyelitisHaematopoietic stem cellsFc fusion proteinMultiple sclerosisAnimal modelsExperimental autoimmune encephalomyelitis lesionsCNS-infiltrating macrophagesStem cellsMultiple sclerosis modelInflammatory cell infiltrateNogo receptor 1Spinal cord injuryContext of neuroinflammationRecipient female miceImmune cell lineagesHigh-affinity receptorDisease-specific mannerDifferentiated phagocytesNeurological recoveryExtensive demyelinationAxonal damageCell infiltrateCNS lesionsNeurological decline
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