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Tumor associated myeloid cells support CNS invasive murine T-cell acute lymphoblastic leukemia

ABSTRACT: Tumor associated myeloid cells support CNS invasive murine T-cell acute lymphoblastic leukemia

PROVIDER: PRJNA1154641 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30494890_1.fastq.gz	Fastqsanger.gz
	SRR30494890_2.fastq.gz	Fastqsanger.gz
	SRR30494891_1.fastq.gz	Fastqsanger.gz
	SRR30494891_2.fastq.gz	Fastqsanger.gz
	SRR30494892_1.fastq.gz	Fastqsanger.gz

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Tumor associated myeloid cells support CNS invasive murine T-cell acute lymphoblastic leukemia

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Sex-specific control of CNS autoimmunity by p38 MAPK signaling in myeloid cells

Project description:Objective: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS), characterized by a global increasing incidence driven by relapsing-remitting disease in females. p38 MAP kinase (MAPK) has been described as a key regulator of inflammatory responses in autoimmunity, but its role in the sexual dimorphism in MS or MS models remains unexplored. Methods: Toward this end, we used experimental autoimmune encephalomyelitis (EAE), the principal animal model of MS, combined with pharmacologic and genetic inhibition of p38 MAPK activity and transcriptomic analyses. Results: Pharmacologic inhibition of p38 MAPK selectively ameliorated EAE in female mice. Conditional deletion studies demonstrated that p38M-NM-1 signaling in macrophages/myeloid cells, but not T cells or dendritic cells, recapitulated this sexual dimorphism. Analysis of CNS inflammatory infiltrates showed that female, but not male mice lacking p38M-NM-1 in myeloid cells exhibited reduced immune cell activation compared with controls, while peripheral T cell priming was unaffected in both sexes. Transcriptomic analyses of myeloid cells revealed differences in p38M-NM-1-controlled transcripts comprising female- and male-specific gene modules, with greater p38M-NM-1 dependence of pro-inflammatory gene expression in females. Interpretation: Our findings demonstrate a key role for p38M-NM-1 in myeloid cells in CNS autoimmunity and uncover important molecular mechanisms underlying sex differences in disease pathogenesis. Taken together, our results suggest that the p38 MAPK signaling pathway represents a novel target for much needed disease modifying therapies for MS WT vs. p38alphaCKO macrophages, male vs. female

2013-10-29 | E-GEOD-51707 | biostudies-arrayexpress

Myeloid lineage C3 induces reactive gliosis and neuronal stress during CNS inflammation

Project description:Complement component C3 mediates pathology in several CNS neurodegenerative diseases, but the cellular and molecular mechanisms leading to neuronal injury remain unclear. We examined how C3 deletion affects glial profiles and anterior visual pathway pathology in an animal model of neuroinflammation, EAE. scRNA-seq from mouse brain and optic nerve revealed that C3 expression defined disease-associated glial subtypes characterized by increased expression of genes associated with mTOR activation, cell metabolism, and translation. This was confirmed with proteomic analysis of the optic nerves of C3KO and WT EAE mice. Deletion of C3 restored glia towards homeostatic profiles. Myeloid-derived C3 mediated injury in optic nerve axons and retinal ganglion cells (RGCs) at disease peak. Our study supports a direct role for C3 in activating the mTOR-ribosomal biogenesis axis in glia which subsequently mediate early neuro-axonal stress and synapse loss.

2025-02-17 | PXD054869 | Pride

Sex-specific control of CNS autoimmunity by p38 MAPK signaling in myeloid cells

Project description:Objective: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS), characterized by a global increasing incidence driven by relapsing-remitting disease in females. p38 MAP kinase (MAPK) has been described as a key regulator of inflammatory responses in autoimmunity, but its role in the sexual dimorphism in MS or MS models remains unexplored. Methods: Toward this end, we used experimental autoimmune encephalomyelitis (EAE), the principal animal model of MS, combined with pharmacologic and genetic inhibition of p38 MAPK activity and transcriptomic analyses. Results: Pharmacologic inhibition of p38 MAPK selectively ameliorated EAE in female mice. Conditional deletion studies demonstrated that p38α signaling in macrophages/myeloid cells, but not T cells or dendritic cells, recapitulated this sexual dimorphism. Analysis of CNS inflammatory infiltrates showed that female, but not male mice lacking p38α in myeloid cells exhibited reduced immune cell activation compared with controls, while peripheral T cell priming was unaffected in both sexes. Transcriptomic analyses of myeloid cells revealed differences in p38α-controlled transcripts comprising female- and male-specific gene modules, with greater p38α dependence of pro-inflammatory gene expression in females. Interpretation: Our findings demonstrate a key role for p38α in myeloid cells in CNS autoimmunity and uncover important molecular mechanisms underlying sex differences in disease pathogenesis. Taken together, our results suggest that the p38 MAPK signaling pathway represents a novel target for much needed disease modifying therapies for MS

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2023-03-11 | PXD022411 | Pride

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