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- W4313385502 abstract "Abstract Infections have been implicated in playing a role in autoimmune diseases. Most reports discuss infectious insults as an initiator of autoimmune disease. Despite the idea that microbes act as triggers for autoimmune disease, their direct role in multiple sclerosis for example is still a topic of debate. Instead of assessing the role of infection in initiating disease, we address the converse hypothesis and test whether some infections can have protective effects. We investigated the role of LCMV infection during the well-established C57Bl/6 EAE model of chronic-progressive disease. In our model, mice infected with LCMV had a delay in EAE disease course compared to uninfected controls with significantly fewer myelin tetramer positive CD4 T cells in the CNS. However, roughly equal numbers of myelin-specific T cells were seen in the periphery suggesting that absence in the CNS was not due to lack of antigen-specific expansion. The CNS was instead populated with LCMV specific CD8 T cells. Therefore, EAE disease course is delayed during LCMV infection as a result of a lack of myelin-specific T cell homing into the CNS and the characteristic neuroinflammation mediated by this T cell population." @default.
- W4313385502 created "2023-01-06" @default.
- W4313385502 creator A5062829620 @default.
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- W4313385502 date "2016-05-01" @default.
- W4313385502 modified "2023-09-26" @default.
- W4313385502 title "LCMV infection prevents MOG-specific T cell trafficking to the CNS and delays EAE" @default.
- W4313385502 doi "https://doi.org/10.4049/jimmunol.196.supp.118.17" @default.
- W4313385502 hasPublicationYear "2016" @default.
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