| Project/Area Number |
03807051
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | National Institute of Neuroscience, NCNP |
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Principal Investigator |
YAMAMURA Takashi National Institute of Neuroscience, NCNP. Division of Demyelinating Disease and Aging. Section chief, 神経研究所・第6部, 室長 (90231670)
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| Co-Investigator(Kenkyū-buntansha) |
SATOH Jun-ichi National Institute of Neuroscience, NCNP. Division of Demyelinating Disease and, 神経センター・神経研究所・第6部, 外来研究員
KUNISHITA Tatsuhide National Institute of Neuroscience, NCNP. Division of Demyelinating Disease and, 神経センター・神経研究所・第6部, 室長 (40167383)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1992: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | T cell growth factor / Oligodendrocyte / O-2A progenitor / Interleukin-2 / O-2A 前駆細胞 / インターロイキン 2 / 0ー2A前駆細胞 / T細胞増殖因子 / 細胞間相互作用 |
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| Research Abstract |
We analyzed cellular interactions between T lymphocytes and a recently established immortalized glial line, L3 that retains several properties of immature oligodendrocytes (Aloisi et al., J Neurosci Res 27 : 16-24, 1990). L3 oligodendrocytes (L3-OL) cannot be induced to express class II antigens, nor do they specifically present antigen to syngeneic specific T lymphocyte. However, L3-OL strongly enhance the proliferation of freshly activated, interleukin-2 (IL-2)-dependent T line lymphocytes and concanavalin A (ConA)-activated lymphoblasts, irrespective of their antigen specificity of surface phenotype (CD4+ or CD8+). The mitogen-ic effect of L3-OL was observed in paraformaldehyde-fixed L3-OL cells and in membrane preparations, but not in culture supernatant. Neither intact L3-OL cells nor membrane preparations had direct IL-2 activity. The conclusion that the mitogenic effect of L3-OL cells is exerted by membrane structures acting as a costimulatory factor(s) of IL-2 is supported by the finding that it is largely blocked by a monoclonal anti-IL-2 receptor antibody. The effect is distinct from membrane-bound IL-1, membrane-bound tumor necrosis factor-alpha, IL-3, or IL-6 and cannot be reconstituted by these cytokines.
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