The suppression of T cell apoptosis influences the severity of disease during the chronic phase but not the recovery from the acute phase of experimental autoimmune encephalomyelitis in mice

Yoshinobu Okuda, Misa Okuda, Claude Charles Andre Bernard

    Research output: Contribution to journalArticleResearchpeer-review

    30 Citations (Scopus)


    The elimination of T cells by apoptosis is considered to be one of the regulatory factors in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. To address further the role of apoptotic T cell death in EAE, we investigated myelin oligodendrocyte glycoprotein (MOG)-induced EAE in transgenic mice overexpressing the anti-apoptotic gene, bcl-2, in T cells. During the acute phase of EAE, no significant difference was observed in the clinical course, pathology and T cell response to MOG between bcl-2 transgenic mice and wild-type littermates. While the recovery from the first attack of EAE was not impaired in the bcl-2 transgenic mice, a more severe disease was observed during the chronic phase of the disease even though T and B cell responses to MOG were comparable to those of wild-type littermates. A flow cytometric analysis by Annexin V showed a significant decrease of apoptotic T cells in the central nervous system (CNS) of the bcl-2 transgenic mice with EAE compared with controls during the chronic as well as the acute phase of disease. These results suggest that while T cell apoptosis in the CNS may play a regulatory role in EAE, the spontaneous recovery from acute EAE cannot solely be explained by T cell apoptosis.
    Original languageEnglish
    Pages (from-to)115 - 125
    Number of pages11
    JournalJournal of Neuroimmunology
    Issue number1-2
    Publication statusPublished - 2002

    Cite this