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[On the mechanisms of human T cell proliferation induced by the 10B4 molecule].

作者信息

Katayama K, Kobata T, Katagiri M

机构信息

Second Department of Pathology, Asahikawa Medical College, Hokkaido, Japan.

出版信息

Hokkaido Igaku Zasshi. 1987 Dec;62(6):866-72.

PMID:3127316
Abstract

The 10B4 system of human T cells seems to constitute a member of T cell receptor complex. We have analyzed the mechanisms by which a monoclonal antibody against the 10B4 molecule activates human peripheral T cells. The 10B4 antibody together with goat anti-mouse immunoglobulin antibody induced significant increase of DNA and RNA syntheses in T cells with peak responses on day 9 and on day 7, respectively. This activation process is mediated by interleukin 2 (IL-2) and its receptor (IL-2R), because (1) IL-2 activity was detected in the culture supernatants, (2) the percentage of IL-2R positive cells increased during the culture period, with a peak on day 9, and (3) the 10B4-induced T cell proliferation was inhibited by anti IL-2R antibody. Blocking studies with pharmacological agents showed that in the 10B4-induced system, a protein kinase C (PK-C) inhibitor, palmitoylcarnitine, blocked DNA synthesis, RNA synthesis, IL-2 production and IL-2R expression whereas a Ca ion channel blocker, verapamil, inhibited DNA synthesis, RNA synthesis, IL-2 production but not IL-2R expression. It is thus concluded that PK-C activation is required for IL-2 production and IL-2R expression and that channel-mediated Ca ion influx is important for IL-2 production but may not be needed for IL-2R expression.

摘要

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