Spelling suggestions: "subject:"autoimmune encephalitis""
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Antigen-dependent regulation of cytokine and chemokine expression in EAELassmann, Silke January 1998 (has links)
No description available.
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Live imaging of autoimmune responses in distinct milieus of the central nervous systemSchlosser, Corinna 14 June 2013 (has links)
No description available.
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Angiogenesis as a pathologic mechanism and novel therapeutic target in an animal model of multiple sclerosisMacMillan, Carolyn Jo-Anne 04 March 2013 (has links)
Multiple sclerosis (MS) is an inflammatory autoimmune disease of the central
nervous system. We hypothesize that angiogenesis results in new vessels which serve as a
conduit for immune cell recruitment in MS, and contribute to inflammation through the
pro-inflammatory properties of angiogenic regulators. This study is one of the first to
explore regulation of angiogenesis in a murine model of MS (experimental autoimmune
encephalomyelitis, EAE), and its potential as a therapeutic target.
Angiogenesis was apparent 21 days following disease induction and correlated with
clinical and pathologic scores. We documented alterations in the VEGF and Ang/Tie
signaling pathways. Expression of VEGF increased at day 14 then reduced by day 21. At
this time point, Ang-2 levels were elevated due to expression by infiltrating macrophages.
Ang-1 was significantly reduced at day 14 and increased at day 21 due to expression by
CD3+ T-cells. The same expression pattern was validated in inflammatory cells within
human MS tissue. Vascular permeability increased at day 14 and returned to control
levels at day 21. The volume of permeable tissue weakly correlated with angiogenesis.
VEGF blockage with bevacizumab suppressed angiogenesis and reduced clinical
scores and vascular permeability. Retention of CD4+ T-cells in peripheral lymph nodes
and reduced T-cell proliferation was noted following treatment. Bevacizumab reduced
mononuclear cell infiltration into spinal cord. Isolated CD4+ T-cells showed reduced
expression of IL-17 and IFN-??. B20-4.1.1 (a monoclonal antibody against murine VEGF)
reduced clinical scores and suppressed angiogenesis as did treatment with angiostatin (an
inhibitor of endothelial cell proliferation). B20-4.1.1 reduced vascular permeability,
induced retention of CD4+ T-cells in peripheral lymph nodes, and inhibited T-cell
proliferation, while angiostatin had no effect. Isolated lymphoid cells from mice treated
with both agents showed reduced secretion of IL-17, but B20-4.1.1 had no effect on Tcell
proliferation or IL-17 secretion when combined with angiostatin. ??
We conclude that these angiogenesis inhibitors are effective in EAE and act by
suppressing angiogenesis with a secondary effect on peripheral T-cell activation. To the
extent that EAE replicates changes occurring in MS, we have demonstrated that
modulation of angiogenesis may represent a promising strategy in the management of
disease progression.
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Autoimmune T cell - B cell interaction in experimental autoimmune encephalomyelitisFlach, Anne-Christine 09 July 2014 (has links)
No description available.
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The influence of common infections on clinical course and neurodegeneration in an animal model of multiple sclerosisKumar, Prateek 07 September 2014 (has links)
No description available.
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Elucidating the mechanisms of disease-triggering myelin-specific autoantibodiesStrauß, Judith 19 March 2020 (has links)
No description available.
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Functional Roles of Peroxisome Proliferator-Activated Receptor β/δ in a Model of Relapsing-Remitting Experimental Autoimmune EncephalomyelitisMadusha Peiris Unknown Date (has links)
Multiple sclerosis (MS) is a chronic neurodegenerative disease characterized by lesions that form within the central nervous system which induce symptoms such as muscle weakness and paralysis. Many aspects of MS, ranging from causation to immunopathology, are currently under investigation as little is known of the factors that contribute to and exacerbate this disease. Presently, evidence suggests MS to be an inflammatory disease mediated by an autoimmune response to an unknown antigen. Results from clinical studies as well as animal models such as experimental autoimmune encephalomyelitis (EAE) suggest MS is initiated and maintained by immune cells such as Th1 lymphocytes. As a result, therapeutics prescribed to MS patients’ focus on modulating the inflammatory response so as to minimize myelin loss and CNS damage. Peroxisome proliferator-activated receptors (PPARs) are a family of transcription factors that show promise as potential targets for MS therapeutics. The PPAR sub-types, PPARα and PPARγ, have been shown to inhibit the propagation of inflammatory pathways and decrease the activity of pro-inflammatory cells in a number of inflammation driven diseases including rheumatoid arthritis and atherosclerosis. The anti-inflammatory role of PPARβ/δ is less well known, although preliminary studies suggest activation of this receptor may potentiate the activity of other transcription factors involved in inhibiting inflammatory pathways. As the PPAR family of transcription factors exhibit similar functions, it is hypothesized that the PPARβ/δ sub-type may have immunomodulatory effects that are comparable and complimentary to PPARα and –γ. This thesis describes a novel model of relapsing-remitting EAE (RR-EAE) that presents a disease course where EAE relapses are followed by periods of recovery that are characterized by the absence of clinical symptoms. Furthermore, a therapeutic intervention study carried out using this model demonstrates that the PPARγ agonist pioglitazone can decrease the severity of a relapse episode when drug treatment begins prior to a predicted relapse event. The inhibition of immune cell infiltration into the CNS and decreased immune cell activity mediated by pioglitazone, suggests that this ligand modulates the immune response. These results indicate that pioglitazone may be an effective treatment for relapsing-remitting MS. To examine the role of PPARβ/δ in RR-EAE and explore its effect on the activity of inflammatory cells, PPARβ/δ knockout mice were used due to the current lack of specific antagonists for this receptor. PPARβ/δ wild-type mice developed RR-EAE when immunized using protocol intended to induce this disease course. PPARβ/δ knockout mice however, developed chronic EAE when immunized in the same manner. Consistent with sustained clinical symptoms, CNS immune cell infiltration and activity was maintained throughout the disease in PPARβ/δ knockout mice. In contrast, the presence of immune cells within the CNS and consequent activity fluctuated according to the relapse and recovery pattern of disease in PPARβ/δ wild-type mice. PPARβ/δ appears to modulate inflammation by potentiating the apoptosis of activated T cells. Therefore, PPARβ/δ agonists may be potential candidates for MS treatment.
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Die Rolle des antiapoptotischen Gens Gimap5 für die Pathogenese neuroinflammatorischer Erkrankungen / The role of the antiapoptotic gene Gimap5 on the pathogenesis of neuroinflammatory diseasesWitte, Ann-Kathrin 09 November 2017 (has links)
No description available.
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The Response of the Glycerophosphocholine Metabolite Lipidome to Experimental Autoimmune Encephalomyelitis and Cycling Female Sex Hormones in the Hippocampus and Temporal-Parietal-Entorhinal Cortex of Female MiceSherman, Samantha January 2016 (has links)
Recently, several glycerophosphocholine biomarkers for multiple sclerosis were discovered in serum, plasma, and cerebrospinal fluid; little is known, however, about brain glycerophosphocholine metabolism during multiple sclerosis despite evidence that lysophosphocholines can elicit demyelination experimentally. Using a lipidomics approach, glycerophosphocholine metabolites in the hippocampus and temporal-parietal-entorhinal cortex of female C57BL/6J mice subjected to experimental autoimmune encephalomyelitis (a mouse model of multiple sclerosis) were quantified and compared to metabolite levels in healthy mice. To control for potential hormonal regulation, glycerophosphocholine metabolites from these same regions were quantified across the estrous cycle in healthy female N5 C57BL/6J x C3h/HeJ mice. I found that several critical glycerophosphocholine metabolites were significantly decreased over the course of experimental autoimmune encephalomyelitis in both brain regions, although the hippocampus was more affected compared to the temporal-parietal-entorhinal cortex. Similarly, hippocampal glycerophosphocholine metabolism was more responsive to fluctuations in female sex hormones than the cortex. Overall, these results suggest that glycerophosphocholine metabolism differs not only between brain regions, but also between conditions, namely experimental autoimmune encephalomyelitis and the estrous cycle.
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The role of the lung in shaping CNS autoimmunityHosang, Leon 01 July 2019 (has links)
No description available.
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