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      • Poster Session : PS 0011 ; Immunology : FTY720 Binds to Affi nity For G Protein-Coupled Sphingosine- 1-Phosphate on Lymphocytes, Inhibiting CD+4 CD+8 T-Cells and B-Cells Thought to Prevent CNS for Reduction of Relapsing-Remitting Multiple Sclerosis

        ( Soonei Hwangbo ),( Sunyi Hwangbo ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1

        Background: Multiple Sclerosis (MS) is a progressive neurologic illness is thought to trigger an autoimmune response that leads ultimately to demyelination in the central nervous system (CNS). restricting lymphocytes to be a FTY720-dependent decrease the internalization of S1P1 renders these cells unresponsive to S1P depriving lymphocytes of the obligatory signal to egress of lymphocytes from lymphoid tissue and thus reduction of auto-aggressive T-lymphocytes in the peripheral recirculation and the central nervous system actions that are mediated by the S1P1 receptor subtype down-modulation causes a reversible retention of a proportion of CD4 and CD8 positive T-cells and B-cells from blood and spleen into lymph nodes could be of benefi t. Methods: The objective was to compare two doses of FTY720 (1.25 mg and 0.5 mg) with annualized relapse rate (ARR), the Expanded Disability Status Scale(EDSS) in patients treated for up to 24 months. Results: Immune function Blood and spleen samples were taken in Weeks 42-43 for in vitro analysis of the immune function. the proliferative responses of B- and T-cells were suppressed at both doses by 52.1-96% and 88.9-97.2% compared to control animals. In trial D2301, treatment of both doses of FTY720 1.25 mg and 0.5 mg resulted in a signifi cantly lower aggregate ARR compared to placebo, with ARR estimates of 0.16 and 0.18 vs. 0.40 respectively. treatment with both doses of FTY720 1.25 mg (p=0.012) and 0.5 mg(p=0.024) resulted in a signifi cantly reduced risk of disability progression compared to treatment with placebo in patients with RRMS. Conclusions: This review provides an overview of our understanding of CD8+ T cells in immune-mediated disease, focusing particularly on our fi ndings regarding regulatory CD8+T cells both in MS and in EAE.

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