Immunity

Journal: Immunity

Publisher

Elsevier

ISSN

1074-7613
1097-4180

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Publications 1 - 7 of 7

Interleukin-34-dependent perivascular macrophages promote vascular function in the brain
Van Hove, Hannah; Glück, Chaim; Mildenberger, Wiebke; et al. (2025)
Immunity
The development of most macrophages depends on the colony-stimulating factor 1 (CSF-1) receptor, which has two ligands: CSF-1 and interleukin-34 (IL-34). While IL-34 is required for the homeostasis of microglia, the parenchymal macrophages in the central nervous system (CNS), it is unclear whether brain border-associated macrophages (BAMs) also depend on this cytokine. Here, we demonstrated that the embryonic development of murine BAMs in the choroid plexus, leptomeninges, and perivascular spaces required CSF-1, while IL-34 was critical for their maintenance in adulthood. In the brain, Il34 was expressed by mural cells and perivascular fibroblasts, and its transgenic deletion in these cells interrupted BAM maintenance. Il34 deficiency coincided with transcriptional changes in vascular cells, leading to increased flow velocity and vasomotion in pial and penetrating arterioles. Similarly, Mrc1$^{Cre}$Csf1r$^{fl/fl}$ mice lacking CD206$^+$ perivascular BAMs exhibited increased hemodynamics in arterial networks. These findings reveal a crosstalk between vascular cells and CNS macrophages regulating cerebrovascular function.
The Microglial Innate Immune Receptor TREM2 Is Required for Synapse Elimination and Normal Brain Connectivity
Filipello, Fabia; Morini, Raffaella; Corradini, Irene; et al. (2018)
Immunity
Cre-Mediated Cell Ablation Contests Mast Cell Contribution in Models of Antibody- and T Cell-Mediated Autoimmunity
Feyerabend, Thorsten B.; Weiser, Anne; Tietz, Annette; et al. (2011)
Immunity
Inflammasome Regulates Hematopoiesis through Cleavage of the Master Erythroid Transcription Factor GATA1
Tyrkalska, Sylwia D.; Pérez-Oliva, Ana B.; Rodríguez-Ruiz, Lola; et al. (2019)
Immunity
Interleukin-17-Producing γδ T Cells Originate from SOX13+ Progenitors that Are Independent of γδTCR Signaling
Spidale, Nicholas A.; Sylvia, Katelyn; Narayan, Kavitha; et al. (2018)
Immunity
Autoimmune Th17 Cells Induced Synovial Stromal and Innate Lymphoid Cell Secretion of the Cytokine GM-CSF to Initiate and Augment Autoimmune Arthritis
Hirota, Keiji; Hashimoto, Motomu; Ito, Yoshinaga; et al. (2018)
Immunity
Despite the importance of Th17 cells in autoimmune diseases, it remains unclear how they control other inflammatory cells in autoimmune tissue damage. Using a model of spontaneous autoimmune arthritis, we showed that arthritogenic Th17 cells stimulated fibroblast-like synoviocytes via interleukin-17 (IL-17) to secrete the cytokine GM-CSF and also expanded synovial-resident innate lymphoid cells (ILCs) in inflamed joints. Activated synovial ILCs, which expressed CD25, IL-33Ra, and TLR9, produced abundant GM-CSF upon stimulation by IL-2, IL-33, or CpG DNA. Loss of GM-CSF production by either ILCs or radio-resistant stromal cells prevented Th17 cell-mediated arthritis. GM-CSF production by Th17 cells augmented chronic inflammation but was dispensable for the initiation of arthritis. We showed that GM-CSF-producing ILCs were present in inflamed joints of rheumatoid arthritis patients. Thus, a cellular cascade of autoimmune Th17 cells, ILCs, and stromal cells, via IL-17 and GM-CSF, mediates chronic joint inflammation and can be a target for therapeutic intervention.
ATP-Gated Ionotropic P2X7 Receptor Controls Follicular T Helper Cell Numbers in Peyer's Patches to Promote Host-Microbiota Mutualism
Proietti, Michele; Cornacchione, Vanessa; Rezzonico Jost, Tanja; et al. (2014)
Immunity

Publications 1 - 7 of 7

Journal: Immunity

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