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B细胞刺激因子1(白细胞介素4)对人外周血溶细胞性细胞群体的调节

Regulation of cytolytic cell populations from human peripheral blood by B cell stimulatory factor 1 (interleukin 4).

作者信息

Widmer M B, Acres R B, Sassenfeld H M, Grabstein K H

机构信息

Immunex Corporation, Seattle, Washington 98101.

出版信息

J Exp Med. 1987 Nov 1;166(5):1447-55. doi: 10.1084/jem.166.5.1447.

Abstract

The effects of B cell stimulatory factor 1 (BSF-1) on the generation of human CTL and lymphokine-activated killer (LAK) cells in vitro were investigated. Both L-2 and BSF-1 were potent helper factors for the generation of antigen-specific CTL in MLC; detection of optimal BSF-1-induced CTL activity in this system occurred when BSF-1 was added to cultures after an initial period of activation during which exogenous BSF-1 was not present. In contrast to IL-2, BSF-1 failed to induce an LAK cell population, as detected with Daudi tumor targets, in cultures that had not been allosensitized. Furthermore, when both lymphokines were added together at culture initiation, BSF-1 inhibited the IL-2-driven generation of cytolytic cells. The differential ability of BSF-1 to promote the generation of CTL but not LAK could have important implications for lymphokine-mediated immunotherapy.

摘要

研究了B细胞刺激因子1(BSF-1)对体外人细胞毒性T淋巴细胞(CTL)和淋巴因子激活的杀伤(LAK)细胞生成的影响。白细胞介素-2(IL-2)和BSF-1都是混合淋巴细胞培养(MLC)中抗原特异性CTL生成的有效辅助因子;在该系统中,当在初始激活期(在此期间不存在外源性BSF-1)后向培养物中添加BSF-1时,可检测到最佳的BSF-1诱导的CTL活性。与IL-2相反,在未进行同种异体致敏的培养物中,如用Daudi肿瘤靶标检测到的那样,BSF-1未能诱导LAK细胞群体。此外,当在培养开始时同时添加这两种淋巴因子时,BSF-1抑制了IL-2驱动的溶细胞性细胞的生成。BSF-1促进CTL生成而不促进LAK生成的不同能力可能对淋巴因子介导的免疫治疗具有重要意义。

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