{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/95505"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/95505","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Upper-respiratory infection triggers experimental autoimmune encephalomyelitis onset in autoimmune prone t-cell receptor transgenic mice","abstract":"Multiple Sclerosis (MS) is an autoimmune-mediated demyelinating and neurodegenerative disease of the central nervous system. Most MS patients experience a disease course characterized by periods of symptom exacerbation (relapses) followed by periods of partial recovery (remission). Relapse contributes to disability but the processes that trigger relapses are poorly understood. Upper-respiratory viral infection increases the risk for relapse. Here, we tested the hypothesis that upper respiratory infection is sufficient to cause glial activation, promote immune cell trafficking to the CNS and trigger pathology in an autoimmune-prone T cell receptor transgenic mouse line. To test this hypothesis we infected 2D2 mice and monitored for symptoms of inflammatory demyelination (EAE). Clinical and histological EAE was observed in ~29.2% of infected 2D2 mice which closely resembles the incidence of upper-respiratory infection-induced relapse in MS patients. Chemokine production in brain resident glial cells, primarily astrocytes was induced by TNF and IL-1β stimulation which may assist in the trafficking of immune cells to the CNS. Furthermore, pharmacological inhibitors of JNK, ERK1/2, p38, and NF-κB modulated the levels of chemokines secreted by astrocytes in response to cytokine stimulation. Increased levels of serum IFN-γ were observed in C57BL/6 mice infected with influenza as well as increased CD4+ T-cells in the choroid plexus. Finally, we observed immunosurveillance of the brain by T-cells and CD45highCD11b+ cells in C57BL/6 mice after influenza inoculation. This immunosurveillance could prove detrimental to MS patients.","abstract_html":"Multiple Sclerosis (MS) is an autoimmune-mediated demyelinating and neurodegenerative disease of the central nervous system. Most MS patients experience a disease course characterized by periods of symptom exacerbation (relapses) followed by periods of partial recovery (remission). Relapse contributes to disability but the processes that trigger relapses are poorly understood. Upper-respiratory viral infection increases the risk for relapse. Here, we tested the hypothesis that upper respiratory infection is sufficient to cause glial activation, promote immune cell trafficking to the CNS and trigger pathology in an autoimmune-prone T cell receptor transgenic mouse line. To test this hypothesis we infected 2D2 mice and monitored for symptoms of inflammatory demyelination (EAE). Clinical and histological EAE was observed in ~29.2% of infected 2D2 mice which closely resembles the incidence of upper-respiratory infection-induced relapse in MS patients. Chemokine production in brain resident glial cells, primarily astrocytes was induced by TNF and IL-1β stimulation which may assist in the trafficking of immune cells to the CNS. Furthermore, pharmacological inhibitors of JNK, ERK1/2, p38, and NF-κB modulated the levels of chemokines secreted by astrocytes in response to cytokine stimulation. Increased levels of serum IFN-γ were observed in C57BL/6 mice infected with influenza as well as increased CD4+ T-cells in the choroid plexus. Finally, we observed immunosurveillance of the brain by T-cells and CD45highCD11b+ cells in C57BL/6 mice after influenza inoculation. This immunosurveillance could prove detrimental to MS patients.","abstract_has_math":false,"creators":["Blackmore, Stephen Daniel"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"M.S.","degree_level":"Thesis","degree_discipline":"Animal Sciences","degree_department":null,"school":null,"contributors":["Steelman, Andrew J.","Gaskins, H. 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Most MS patients experience a disease course characterized by periods of symptom exacerbation (relapses) followed by periods of partial recovery (remission). Relapse contributes to disability but the processes that trigger relapses are poorly understood. Upper-respiratory viral infection increases the risk for relapse. Here, we tested the hypothesis that upper respiratory infection is sufficient to cause glial activation, promote immune cell trafficking to the CNS and trigger pathology in an autoimmune-prone T cell receptor transgenic mouse line. To test this hypothesis we infected 2D2 mice and monitored for symptoms of inflammatory demyelination (EAE). Clinical and histological EAE was observed in ~29.2% of infected 2D2 mice which closely resembles the incidence of upper-respiratory infection-induced relapse in MS patients. Chemokine production in brain resident glial cells, primarily astrocytes was induced by TNF and IL-1β stimulation which may assist in the trafficking of immune cells to the CNS. Furthermore, pharmacological inhibitors of JNK, ERK1/2, p38, and NF-κB modulated the levels of chemokines secreted by astrocytes in response to cytokine stimulation. Increased levels of serum IFN-γ were observed in C57BL/6 mice infected with influenza as well as increased CD4+ T-cells in the choroid plexus. Finally, we observed immunosurveillance of the brain by T-cells and CD45highCD11b+ cells in C57BL/6 mice after influenza inoculation. 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Clinical and histological EAE was observed in ~29.2% of infected 2D2 mice which closely resembles the incidence of upper-respiratory infection-induced relapse in MS patients. Chemokine production in brain resident glial cells, primarily astrocytes was induced by TNF and IL-1β stimulation which may assist in the trafficking of immune cells to the CNS. Furthermore, pharmacological inhibitors of JNK, ERK1/2, p38, and NF-κB modulated the levels of chemokines secreted by astrocytes in response to cytokine stimulation. Increased levels of serum IFN-γ were observed in C57BL/6 mice infected with influenza as well as increased CD4+ T-cells in the choroid plexus. Finally, we observed immunosurveillance of the brain by T-cells and CD45highCD11b+ cells in C57BL/6 mice after influenza inoculation. This immunosurveillance could prove detrimental to MS patients.","Submission published under a 24 month embargo labeled 'U of I Access', the embargo will last until 2018-12-01","The student, Stephen Blackmore, accepted the attached license on 2016-12-02 at 08:12.","The student, Stephen Blackmore, submitted this Thesis for approval on 2016-12-02 at 08:19.","This Thesis was approved for publication on 2016-12-05 at 14:10.","DSpace SAF Submission Ingestion Package generated from Vireo submission #10412 on 2017-02-28 at 14:37:13","Made available in DSpace on 2017-03-01T16:37:05Z (GMT). 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