Project/Area Number |
09670688
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neurology
|
Research Institution | Osaka University |
Principal Investigator |
YAMAMOTO Hiroshi Graduate School of Pharmaceutical Sciences, Immunology, Osaka University, Professor, 薬学研究科, 教授 (50127312)
|
Co-Investigator(Kenkyū-buntansha) |
TSUJIKAWA Kazutake Graduate School of Pharmaceutical Sciences, Immunology, Osaka University, Associate Professor, 薬学研究科, 助手 (10207376)
|
Project Period (FY) |
1997 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1998: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1997: ¥2,000,000 (Direct Cost: ¥2,000,000)
|
Keywords | neuropeptide / T lymphocyte / neuro-immune interaction / cytokine / CGRP / NPY / サイトカイン / 神経ペプチド受容体 / 免疫制御 / ヘルパーT細胞 / ヘルパーT細胞サブセット / 神経-免疫連関 / T細胞サブセット |
Research Abstract |
Though immune outcome is known to be determined by which helper T cell response predominates, no local mechanism has yet been established which can explain how the neuronal system may control this. It is possible that the nervous system releases neuropeptides at specific local sites of infection or challenge, which triggers lymphocytes at those points to release specific cytokine profiles. These may then influence the direction of the Th1/Th2 response and therefore immune outcome. The aim of this study was to evaluate whether and if so how neuropeptides influence cytokine production by lymphocytes, especially T cells. 1 : We investigated the effects of two NPs, neuropeptide Y (NPY) and calcitonin gene-related peptide (CGRP), on the production of interferon-γ(IFNγ) and interleukin-4 (IL-4) by stimulating nonadherent splenocytes and helper T cell clones with antigens in vitro in the presence or absence of these peptides. NPY greatly enhanced IL-4 production and inhibited IFNγ. CGRP inhibited IFNγ production markedly in a dose-dependent manner, but had no effects on IL-4 production. 2 : Both NPY-and CGRP-receptors are expressed on the mouse T lymphocytes. 3 : Stimulation of T lymphocytes with two NPs resulted in an enhanced cAMP-mediated intracellular signaling process. Therefore NPs directly act on T lymphocytes and can influence cytokine production. This opens the door to speculations that these specific cytokine profiles might play a part in influencing the direction of the consequent Th1/Th2 cascade and immune outcome and possibly the pathogenesis of immune-related diseases.
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