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人淋巴细胞体外合成IgE。IV. 衣霉素处理的RPMI 8866细胞分泌的IgE结合因子对自发IgE合成的抑制作用。

In vitro synthesis of IgE by human lymphocytes. IV. Suppression of the spontaneous IgE synthesis by IgE-binding factors secreted by tunicamycin-treated RPMI 8866 cells.

作者信息

Sarfati M, Rector E, Sehon A H, Delespesse G

出版信息

Immunology. 1984 Dec;53(4):783-90.

Abstract

It was previously shown that RPMI 8866 cells released IgE-binding factors (IgE-BFs) capable of enhancing the spontaneous in vitro synthesis of IgE by purified B lymphocytes isolated from allergic individuals. In the present study, the influence of tunicamycin, an inhibitor of protein glycosylation, on RPMI 8866 cells was investigated with regard to: (i) the expression of surface receptors for IgE; (ii) the release of IgE-BFs into the culture supernatants, and (iii) the biological activity of IgE-BFs. After preincubation for 60 min with tunicamycin (1 microgram/ml), RPMI 8866 cells were cultured for 48 hr in HB 101 serum-free medium; the culture supernatant was then filtered, concentrated, and its biological activity was compared to that of a parallel culture supernatant from untreated RPMI 8866 cells. The results of these experiments indicate that exposure of RPMI 8866 cells to tunicamycin resulted in: (i) a reduction of surface Fc epsilon R; (ii) no effect on the release of IgE-BFs into the culture supernatant, and (iii) the conversion of IgE-potentiating factors into IgE-suppressing factors. The latter factors suppressed the IgE secretion by U266 myeloma cells and completely inhibited the activity of IgE-potentiating factors on B lymphocytes from allergic individuals. IgE-BFs secreted by tunicamycin-treated cells had no effect on the production of IgG, IgA or IgM by normal or EBV-transformed B cells.

摘要

先前的研究表明,RPMI 8866细胞可释放IgE结合因子(IgE-BFs),该因子能够增强从过敏个体中分离出的纯化B淋巴细胞体外自发合成IgE的能力。在本研究中,研究了蛋白质糖基化抑制剂衣霉素对RPMI 8866细胞的影响,具体涉及:(i)IgE表面受体的表达;(ii)IgE-BFs释放到培养上清液中的情况;以及(iii)IgE-BFs的生物活性。用衣霉素(1微克/毫升)预孵育60分钟后,将RPMI 8866细胞在HB 101无血清培养基中培养48小时;然后将培养上清液过滤、浓缩,并将其生物活性与未处理的RPMI 8866细胞的平行培养上清液进行比较。这些实验结果表明,RPMI 8866细胞暴露于衣霉素会导致:(i)表面FcεR减少;(ii)对IgE-BFs释放到培养上清液中没有影响;以及(iii)IgE增强因子转化为IgE抑制因子。后一种因子抑制了U266骨髓瘤细胞的IgE分泌,并完全抑制了IgE增强因子对过敏个体B淋巴细胞的活性。经衣霉素处理的细胞分泌的IgE-BFs对正常或EBV转化的B细胞产生IgG、IgA或IgM没有影响。

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