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Interleukin-1 promotes autoimmune neuroinflammation by suppressing endothelial heme oxygenase-1 at the blood-brain barrier

ABSTRACT: The goal of this study is to study endothelial cell Il1r1 signaling in EAE (multiple scleroris)

ORGANISM(S): Mus musculus

PROVIDER: GSE146378 | GEO | 2020/09/23

REPOSITORIES: GEO

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Interleukin-1 promotes autoimmune neuroinflammation by suppressing endothelial heme oxygenase-1 at the blood-brain barrier.

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Interleukin-1 promotes autoimmune neuroinflammation by suppressing endothelial heme oxygenase-1 at the blood-brain barrier

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Oligodendrocyte regulation during autoimmune neuroinflammation

Project description:The present study had the purpose to analyze the transcriptional state of oligodendrocytes in an animal model of multiple scleroris resembling autoimmune neuroinflammation and compared with control mice treated with ovalbumin. The results revealed that oligodendrocytes from the EAE (experimental autoimmune encephalomyelitis) model upregulate genes that are involved in immune processes providing evidence that oligodendrocytes can develop an immune phenotype in particular neuroinflammatory conditions.

2021-08-21 | GSE182341 | GEO

Pathogenic TH17 cells utilize BHLHE40 to instruct myeloid cells during autoimmune neuroinflammation

Project description:TH17 cells are implicated in the pathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). We previously reported that the transcription factor BHLHE40 marks cytokine-producing pathogenic TH cells during EAE, and that its expression in T cells is required for clinical disease. Here, using dual reporter mice, we show BHLHE40 expression within TH1/17 and ex-TH17 cells following EAE induction. Il17a-Cre-mediated deletion of BHLHE40 in TH cells led to less severe EAE with reduced TH cell cytokine production. Characterization of the leukocytes in the central nervous system during EAE by scRNA-sequencing identified differences in the infiltrating myeloid cells when BHLHE40 was present or absent in TH17 cells. Our studies highlight the importance of BHLHE40 in promoting TH17 cell encephalitogenicity and instructing myeloid cell responses during active EAE.

2023-11-01 | GSE234705 | GEO

Oligodendrocyte-derived extracellular vesicles as antigen-specific therapy for autoimmune neuroinflammation

Project description:Autoimmune diseases such as multiple sclerosis (MS) develop because of failed peripheral immune tolerance for a specific self-antigen (Ag). Numerous approaches for Ag-specific suppression of autoimmune neuroinflammation have been proven in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. One such approach is intravenous (i.v.) tolerance induction by injecting a myelin Ag used for EAE induction. However, the translation of this and similar experimental strategies into therapy for MS has been hampered by uncertainty regarding relevant myelin Ags in MS patients. To address this issue, we developed a therapeutic strategy that relies on oligodendrocyte (Ol)-derived extracellular vesicles (Ol-EVs), which naturally contain multiple myelin Ags. Ol-EVs injected i.v. suppressed disease in a myelin Ag-dependent manner, both prophylactically and therapeutically, in several EAE models. The treatment was safe and restored immune tolerance by inducing immunosuppressive monocytes and apoptosis of autoreactive encephalitogenic CD4+ T cells. Finally, we show that human Ols also release EVs containing most relevant myelin Ags, providing a basis for their use in MS therapy. These findings introduce an approach for suppressing central nervous system autoimmunity in a myelin Ag-specific manner.

2020-05-17 | MSV000085434 | MassIVE

A Novel Role for A20-Regulated CNS Endothelial ICOSL in Immune Cell Adhesion and Autoimmune Neuroinflammation

Project description:A20 is a ubiquitin-modifying protein that negatively regulates canonical NF-κB signaling and mutations in A20/TNFAIP3 have been associated with a variety of autoimmune diseases, including multiple sclerosis (MS). We found that deletion of A20 in central nervous system (CNS) endothelial cells (BEC) enhances experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. These mice showed increased numbers of CNS-infiltrating immune cells during neuroinflammation and in the steady state. While the integrity of the barrier was not impaired, we observed a strong activation of the endothelium in A20ΔBEC mice, with dramatically increased levels of the adhesion molecules ICAM-1 and VCAM-1. We furthermore discovered ICOSL as novel adhesion molecule expressed by A20-deficient BECs. Silencing of ICOSL in BECs ameliorated the severity of an active EAE disease in wildtype mice and significantly delayed the onset of symptom development. Furthermore, blocking of ICOSL on primary CNS-derived endothelial cells impaired the adhesion of different T cell populations to the monolayer. Taken together, we here report a novel function of A20-regulated ICOSL expressed on CNS endothelial cells during inflammation. We propose that BEC-ICOSL contributes to the firm adhesion of T cells to the barrier, promoting T cell transmigration into the CNS and eventually driving autoimmune neuroinflammation.

2023-11-03 | GSE221318 | GEO

Serum neurofilament light reveals the contraction from widespread to lesion-bound neuroaxonal injury during autoimmune neuroinflammation

Project description:Blood-based neurofilament light (sNfL) indicates neuroaxonal injury in multiple sclerosis and is on the cusp of being implemented into clinical routine. However, anatomical origins and pathophysiological mechanisms of NfL release during acute relapses and later chronic disease stages are still poorly understood. Here, we applied immunohistochemistry, single molecule array, spatial transcriptomics and microglia/axon co-cultures to gain insight into spatio-temporal NfL release in experimental autoimmune encephalomyelitis (EAE). Results: Association of spinal cord white matter lesions and sNfL levels revealed a distinct, stage-dependent anatomical pattern of neuroaxonal damage: In chronic EAE, sNfL levels were predominately associated with anterolateral lumbar lesions, whereas in early EAE sNfL showed no correlation with lesions in any anatomical location. Furthermore, neuroaxonal damage in late EAE was largely confined to white matter lesions, but showed a widespread distribution in early EAE. Followingthis spatio-temporal pattern of neuroaxonal damage, spatial transcriptomics revealed a widespread cyto- and chemokine response at early disease stages, whereas late EAE was characterized by a prominent glial cell accumulation in white matter lesions. These findings were corroborated by immunohistochemistry and micro-glia/axon co-cultures, which further revealed a strong association between CNS myeloid cell activation and neuroaxonal damage both in vivo and in vitro. Interpretation: Our data demonstrate that sNfL release in EAE driven by CNS myeloid cells exhibits progress in a disease stage-dependent centripetal manner from normal-appearing white matter to focal white matter lesions. These findings may further aid the interpretation of elevated sNfL levels in multiple sclerosis patients at different disease stages.

2023-11-22 | GSE226591 | GEO

The novel RNA binding protein IMP2 drives a stromal-Th17 cell inflammatory circuit in autoimmune neuroinflammation

Project description:Posttranscriptional control of Ccl2 in stromal cells by IMP2 is required to permit IL-17-driven progression of EAE pathogenesis. Using an optimized data analysis workflow, we mapped about 40 million sequence reads per sample to the mouse genome (build mm10) and identified potential differentially regulated transcripts in the lymph nodes of EAE Imp2 KO mice (n=3) compared to EAE WT mice (n=3) with an absolute fold change ≥1.5, p value <0.05 and RPKM in WT mice >1. Altered expression of potential genes was confirmed with qRT–PCR.

2021-07-23 | GSE180561 | GEO

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