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EAF2 deficiency attenuates autoimmune disease in Faslpr mice by modulating B cell activation and apoptosis

ABSTRACT: EAF2 deficiency attenuates autoimmune disease in Faslpr mice by modulating B cell activation and apoptosis

PROVIDER: PRJNA1169839 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30917653.fastq.gz	Fastqsanger.gz
	SRR30917654.fastq.gz	Fastqsanger.gz
	SRR30917655.fastq.gz	Fastqsanger.gz
	SRR30917656.fastq.gz	Fastqsanger.gz
	SRR30917657.fastq.gz	Fastqsanger.gz

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EAF2 deficiency attenuates autoimmune disease in Faslpr mice by modulating B cell activation and apoptosis

Project description:Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that presents significant challenges to human health. MRL/lpr mice, which develop SLE-like autoimmunity due to defective apoptosis in activated B and T cells, were used to study the role of apoptosis in autoimmunity. We generated Faslpr mice deficient in EAF2, a transcription elongation-associated factor known to promote apoptosis in germinal center (GC) B cells and crucial for preventing autoimmunity. Contrary to expectations, EAF2 deficiency significantly reduced lymphadenopathy and splenomegaly, extended lifespan, and alleviated nephritis by decreasing autoantibody production and reducing immune complex deposition in the kidneys. Additionally, EAF2 deficiency markedly reduced accumulation of activated B cells, GC B cells, and plasma cells in Faslpr mice. Moreover, the abnormal B220+CD3+ T cells typically observed in Faslpr mice were substantially reduced by EAF2 deficiency. Further analysis revealed that Eaf2-/-Faslpr B cells showed hyperactivation upon various stimulations, followed by increased death. RNA sequencing of the B220+CD3+ cells revealed a downregulation in survival-promoting genes such as Bcl-2 and Akt and an upregulation of proapoptotic genes. We conclude that the combined deficiency in FAS- and EAF2-mediated apoptotic pathways leads to B cell hyperactivation and subsequent death, thereby ameliorating systemic autoimmunity in this model.

2024-11-20 | GSE278963 | GEO

Gene expression profile of B cells from OPN-competent and deficient Faslpr autoimmune mice

Project description:We performed gene expression profile on splenic CD19+ cells from autoimmune Faslpr/lpr and OPN-/-Faslpr/lpr mice to investigate the dynamics at the basis of the more incident transformation characterizing OPN-deficient animals. GEP on splenic CD19+ from BALB/c and OPN-/- mice was performed as control.

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Endothelial cell-derived oxysterol ablation attenuates experimental autoimmune encephalomyelitis

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METTL16 deficiency attenuates apoptosis through translational control of extrinsic death receptor during nutrient deprivation

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METTL16 deficiency attenuates apoptosis through translational control of extrinsic death receptor during nutrient deprivation

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Quercetin attenuates atherosclerosis via modulating oxidized LDL-induced endothelial cellular senescence

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Endothelial cell-derived oxysterol ablation attenuates experimental autoimmune encephalomyelitis

Project description:The vasculature is a key regulator of leukocyte trafficking into the central nervous system (CNS) during inflammatory diseases including multiple sclerosis. However, the impact of endothelial-derived factors on other aspects of CNS immune responses remains unknown. Bioactive lipids, in particular oxysterols downstream Cholesterol-25-hydroxylase (Ch25h) promote neuroinflammation but their functions in the CNS remain unclear. Using a floxed-reporter Ch25h knock-in mice, we traced Ch25h expression to CNS endothelial cells (ECs) and myeloid cells and demonstrated that Ch25h-specific ablation in ECs attenuates experimental autoimmune encephalomyelitis. Mechanistically, inflamed Ch25h-deficient CNS ECs displayed altered lipid metabolism favoring polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) expansion relative to other leukocyte subsets that suppress encephalitogenic T lymphocytes proliferation. Finally, endothelial Ch25h-deficiency combined with mobilization of immature neutrophils into circulation resulted in nearly complete EAE protection. Our findings reveal a central role for CNS endothelial-derived Ch25h in promoting neuroinflammation by regulating expansion of immunosuppressive myeloid cell populations.

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Magnesium Hexacyanoferrate Nanocatalyst Attenuates Chemodrug-Induced Cardiotoxicity through Ferromodulation-Driven Anti-Apoptosis

Project description:Magnesium Hexacyanoferrate Nanocatalyst Attenuates Chemodrug-Induced Cardiotoxicity through Ferromodulation-Driven Anti-Apoptosis

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Transcription profiling of human peripheral blood mononuclear cells WITH a germline NRAS mutation vs controls reveals NRAScauses a novel human autoimmune lymphoproliferative syndrome (ALPS)

Project description:The p21 RAS subfamily of small GTPases, including KRAS, HRAS, and NRAS, regulates cell proliferation, cytoskeletal organization and other signaling networks, and is the most frequent target of activating mutations in cancer. Activating germline mutations of KRAS and HRAS cause severe developmental abnormalities leading to Noonan, cardio-facial-cutaneous and Costello syndrome, but activating germline mutations of NRAS have not been reported. Autoimmune lymphoproliferative syndrome (ALPS) is the most common genetic disease of lymphocyte apoptosis and causes autoimmunity as well as excessive lymphocyte accumulation, particularly of CD4-, CD8- ab T cells. Mutations in ALPS typically affect CD95 (Fas/APO-1)-mediated apoptosis, one of the extrinsic death pathways involving tumor necrosis factor receptor (TNFR) superfamily proteins, but certain ALPS individuals have no such mutations. We show here that the salient features of ALPS as well as a predisposition to hematological malignancies can be caused by a heterozygous germline Gly13Asp activating mutation of the NRAS oncogene that does not impair CD95-mediated apoptosis. The increase in active, GTP-bound NRAS augments RAF/MEK/ERK signaling which markedly decreases the pro-apoptotic protein BIM and attenuates intrinsic, nonreceptor-mediated mitochondrial apoptosis. Thus, germline activating mutations in NRAS differ from other p21 Ras oncoproteins by causing selective immune abnormalities without general developmental defects. Our observations on the effects of NRAS activation indicate that RAS-inactivating drugs, such as farnesyl-transferase inhibitors (FTIs) should be examined in human autoimmune and lymphocyte homeostasis disorders. Experiment Overall Design: Describes the discovery of a new gene underlying a novel type of autoimmune lymphoproliferative syndrome, and characterizes the mechanisms involved in the pathogenesis of the disease.

2008-04-04 | E-GEOD-7345 | biostudies-arrayexpress

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