Cyclosporin A inhibits late steps of T lymphocyte activation after transmembrane signaling.
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概要
- 論文の詳細を見る
The in vitro stimulation of murine splenic T lymphocytes with concanavalin A (Con A) produced interleukin 2 (IL2). The addition of cyclosporin A (CsA) to the culture resulted in complete inhibition of IL2 production. The Con A stimulation of T lymphocytes induced the breakdown of phosphatidylinositol into inositol trisphosphate and diacylglycerol, each of which could function as the second mes-sengers in the subsequent signal transduction pathway. CsA did not inhibit the production of inositol (poly)phosphates. Further, CsA did not affect Ca2+-calmodulin functions; a) the redistribution of various cytoskeletal proteins as well as Con A-receptor aggregation, and b) the cytosolic Ca2+-calmodulin-dependent en-zyme activities. Moreover, the activity of protein kinase C, which has been accepted to be the target of diacylglycerol, was not influenced in the presence of CsA. While the above steps of signal transduction are bypassed by synergy between calcium ionophore and phorbol ester, T lymphocyte activation which was induced by such stimuli was completely inhibited by CsA. These results indicate that CsA does not influence early steps of T lymphocyte activation as bypassed by calcium ionophore and phorbol ester, but rather inhibits later step(s) subsequent to the activation of protein kinase C and Ca2+-calmodulin.
- 社団法人 日本生化学会の論文
著者
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Fujiwara Hiromi
Department Of Oncology (c6) Graduate School Of Medicine Osaka University
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Itoh Kazuyuki
Department Of Biology Osaka Medical Center For Cancer And Cardiovascular Diseases
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Kosaka Hiroshi
Department Of Applied Chemistry Faculty Of Science And Engineering Saga University
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Yoshida Hiroshi
Departmen Of Radiology School Of Medicine Asahikawa Medical University
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MIZUSHIMA Atsushi
Departments of Pharmacology I, Osaka University School of Medicin
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Osugi Takeshi
Department of Materials Science and Engineering, Kyushu University
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SOBUE Kenji
Department of Neurochemistry and Neuropharmacology, Institute of Higher Nervous Activity, Osaka University Medical School
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HAMAOKA Toshiyuki
Department of Oncogenesis, Institute for Cancer Research
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MIZUSHIMA Yumiko
Department of Oncogenesis, Institute for Cancer Research
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SAKUMA Shozo
Department of Oncogenesis, Institute for Cancer Research
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KANDA Keiko
Department of Neurochemistry and Neuropharmacology, Institute ofHigher Nervous Activity
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