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- W70691921 abstract "Abstract Multiple sclerosis (MS) is a chronic, inflammatory disease of the central nervous system thought to be initiated by CD4+ T cells specific for myelin antigens. Experimental autoimmune encephalomyelitis (EAE), a model of MS, is induced in susceptible mouse strains by immunization with myelin antigens such as myelin oligodendrocyte glycoprotein (MOG). MOG35-55-specific T cell receptor transgenic (2D2) mice are susceptible to EAE following immunization with MOG peptide. To better understand the role of T cells in EAE initiation, we explored several approaches for effecting adoptive transfer of EAE using 2D2 T cells. Surprisingly, despite robust proliferation and production of IFN-γ and IL-17 following a variety of culture conditions, EAE was not transferred. Only when 2D2 whole splenocyte preparations contained CD44+ T cells and were Th1-differentiated using MOG peptide and IL-12 did they reliably transfer EAE. Further, we found that CD44hiCD62Llo effector/memory CD4+ T cells are likely responsible for disease transfer due to up-regulation of the adhesion molecule CD44 following differentiation. We also observed a sex dimorphism in 2D2 mice with males transferring more severe EAE, associated with a larger population of effector/memory CD4+ T cells in males compared to females. Given the importance of MOG in MS pathogenesis, mechanistic insights into adoptively transferred EAE by MOG-specific Th1 cells could prove valuable in MS research." @default.
- W70691921 created "2016-06-24" @default.
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- W70691921 date "2011-04-01" @default.
- W70691921 modified "2023-09-26" @default.
- W70691921 title "Memory cells specific for myelin oligodendrocyte glycoprotein govern the transfer of experimental autoimmune encephalomyelitis (101.26)" @default.
- W70691921 doi "https://doi.org/10.4049/jimmunol.186.supp.101.26" @default.
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