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  • Title: An adhesive glycoprotein from rat ascites hepatoma cells potentiates natural cytotoxic activity by rat spleen cells.
    Author: Chen JY, Kurano R, Hirashima M, Hayashi H.
    Journal: Immunology; 1986 May; 58(1):95-100. PubMed ID: 3710521.
    Abstract:
    In a previous paper, we have described a cell-surface associated adhesive glycoprotein (AF) that has been separated and highly purified from rat ascites hepatoma AH136B cells. AF was found to induce the aggregation and adhesiveness of hepatoma cells. AF was also shown to have a mitogenic activity on rat T lymphocytes, and to stimulate them to produce a lymphokine chemotactic for macrophages. In the present paper, we have examined the effects of AF on natural killing (NK) activity by rat spleen cells against NK-sensitive YAC-1 cells using 51Cr-release cytotoxicity assay. NK activity of spleen cells was potentiated by AF treatment in a dose-dependent manner. A short incubation with AF was sufficient for the potentiation of NK activity, whereas the potentiation by OK-432, which is well known as a potentiator of anti-tumour activity, required a longer stimulation. Macrophage depletion from spleen cells resulted in the decreased potentiating effects of OK-432, whereas the depletion failed to influence the effects of AF. IN subsequent experiments, it was found that AF could potentiate NK activity of the NK-cell enriched fraction. We further found that culture supernatants from spleen cells and peritoneal exudate cells treated with OK-432 potentiate the NK activity, whereas those from AF-treated cells fail. It was thus suggested that AF acts directly on the cells responsible for NK activity, and that the mechanisms of AF-induced potentiation of NK activity differ from those of OK-432-induced potentiation.
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