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淋巴细胞增多促进因子(LPF)、凝集素和地塞米松对人外周血淋巴细胞上IgE受体表达的调节

Regulation of IgE receptor expression on human peripheral blood lymphocytes by lymphocytosis promoting factor (LPF), lectins and dexamethasone.

作者信息

Kim K M, Tanaka M, Yoshimura T, Katamura K, Mayumi M, Mikawa H

机构信息

Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.

出版信息

Clin Exp Immunol. 1987 May;68(2):418-26.

Abstract

Using a monoclonal anti-human Fc epsilon R antibody (H107), we found that lymphocytosis promoting factor (LPF), phytohaemagglutinin (PHA-P) and Concanavalin A (Con A) could induce Fc epsilon R, detected by immunofluorescence study, on normal human peripheral blood lymphocytes without IgE. The number of Fc epsilon R bearing lymphocytes was increased by stimulation with 3, 10 and 10 micrograms/ml of LPF, PHA-P and Con A, respectively, from 6.0 +/- 3.0/1000 cells to 26.0 +/- 7.9, 54.0 +/- 6.7 and 24.8 +/- 7.1/1000 cells, respectively. Although the induction of Fc epsilon R occurred neither in the separated T-enriched fraction (TEF) nor the T-depleted fraction (TDF), it recovered when the two fractions were mixed. The cell free supernatants from TEF stimulated with LPF or PHA-P could increase Fc epsilon R(+) cells in TDF, whereas those from TDF failed to increase them in TEF. The results suggest that the induction of Fc epsilon R occurs mainly on B lymphocytes by the soluble factor(s) formed by T cells stimulated with LPF or PHA-P. The induction of Fc epsilon R by stimulants was completely inhibited by 10(-6) M dexamethasone. It was demonstrated that the effects of dexamethasone on lymphocytes were dual: one was on B cells to inhibit responsive increases of Fc epsilon R, and the other was on T cells to suppress the formation of the soluble factor(s) which induced Fc epsilon R on B cells.

摘要

使用单克隆抗人FcεR抗体(H107),我们发现淋巴细胞增多促进因子(LPF)、植物血凝素(PHA-P)和刀豆球蛋白A(Con A)可诱导正常人外周血淋巴细胞上出现FcεR(通过免疫荧光研究检测),这些淋巴细胞无IgE。分别用3、10和10微克/毫升的LPF、PHA-P和Con A刺激后,携带FcεR的淋巴细胞数量分别从6.0±3.0/1000个细胞增加到26.0±7.9、54.0±6.7和24.8±7.1/1000个细胞。尽管在分离的富含T细胞的部分(TEF)和T细胞耗竭部分(TDF)中均未发生FcεR的诱导,但当将这两个部分混合时,诱导作用恢复。用LPF或PHA-P刺激的TEF的无细胞上清液可增加TDF中FcεR(+)细胞的数量,而TDF的无细胞上清液未能增加TEF中的此类细胞数量。结果表明,FcεR的诱导主要发生在B淋巴细胞上,是由LPF或PHA-P刺激的T细胞形成的可溶性因子所致。10⁻⁶M地塞米松完全抑制了刺激剂对FcεR的诱导作用。已证明地塞米松对淋巴细胞的作用是双重的:一是作用于B细胞以抑制FcεR的反应性增加,另一是作用于T细胞以抑制诱导B细胞上FcεR的可溶性因子的形成。

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