Abstract

Abstract Adoptive transfer of activated central nervous system (CNS) antigen specific T-cells into susceptible strains of mice results in the invasion of transferred cells into the CNS. CNS invasion by these initiating T-cells and recruited monocytes culminates in the induction of experimental autoimmune encephalomyelitis (EAE). Following this initial invasion a secondary infiltrate of host T-cells of unknown function and antigenic specificity enters the CNS. The role of these secondary-infiltrating cells in the initiation, development, and resolution of EAE remains uncharacterized. In this study we utilized an adoptive transfer model of EAE induction in mice to characterize the mechanisms involved in entry of host T-cells found within the CNS following disease initiation. These cells were further examined for both phenotypic and functional characteristics at various times after disease initiation. Finally, we examined the necessity for antigenic recognition of peptides in entry and retention of cells within the CNS. Findings from this study allow us to characterize the mechanisms involved in accumulation of host cells within the CNS during EAE pathogenesis.

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