Lymphokine Production by B Cells from Normal and HIV‐Infected Individuals-猫眼课题宝

正常人和 HIV 感染者 B 细胞产生淋巴因子

DOI：

发表时间：

1992

期刊：

Annals of the New York Academy of Sciences

影响因子：

5.2

通讯作者：

中科院分区：

综合性期刊3区

文献类型：

作者：

J. Kehrl;P. Rieckmann;E. Kozlow;A. Fauci

白细胞介素-6 (IL-6) 和肿瘤坏死因子-α (TNF-α) 均由体内激活的正常 B 细胞和多克隆 B 细胞激活患者体内激活的 B 细胞分泌，包括感染人类免疫缺陷病毒 (HIV) 的个体。此外，IL-6 和 TNF-α 参与人类 B 细胞分化的自分泌和旁分泌调节。用金黄色葡萄球菌 Cowan 菌株 I 和 IL-2 体外刺激正常 B 细胞后，上清液中 TNF-α 水平出现快速但短暂的增加。 IL-6 的产量也有最初的增加，随后是更持续的增加。 IL-6 产量的二次增加取决于 TNF-α 的先前产量。 CD5 阳性与 CD5 阴性扁桃体 B 细胞分泌的 IL-6 和 TNF-α 没有显着差异。正常体外激活的 B 细胞和来自高丙种球蛋白血症患者的新鲜分离的 B 细胞产生的 Ig 在很大程度上取决于 TNF-α 和 IL-6 的产生。作为 B 细胞 TNF-α 和 IL-6 产生的另一种测量方法，从 HIV 感染者中新鲜分离的 B 细胞诱导长期感染 HIV 的细胞产生病毒，已知这些细胞中的 HIV 产生是由多种细胞因子触发的。相比之下，从正常对照中新鲜分离的 B 细胞无法增加 HIV 的产生，除非在体外受到刺激。因此，HIV感染者的B细胞自发产生IL-6和TNF-α可能有助于病毒表达以及通常与HIV感染相关的高丙种球蛋白血症。

Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) are both secreted by in vivo-activated normal B cells and by in vivo-activated B cells from patients with polyclonal B-cell activation, including individuals infected with the human immunodeficiency virus (HIV). Furthermore, IL-6 and TNF-alpha are involved in autocrine and paracrine regulation of human B-cell differentiation. Following in vitro stimulation of normal B cells with Staphylococcus aureus Cowan strain I and IL-2, there is a rapid but brief increase in supernatant levels of TNF-alpha. There is also an initial increase followed by a subsequent and more sustained increase in IL-6 production. The secondary rise in IL-6 production is dependent upon the prior production of TNF-alpha. There is no significant difference in IL-6 and TNF-alpha secretion by CD5 positive versus CD5 negative tonsillar B cells. Ig production by normal in vitro-activated B cells and freshly isolated B cells from patients with hypergammaglobulinemia is largely dependent upon TNF-alpha and IL-6 production. As another measure of B-cell TNF-alpha and IL-6 production, freshly isolated B cells from HIV-infected individuals induce virus production by chronically HIV-infected cells in which HIV production is known to be triggered by a variety of cytokines. By contrast, freshly isolated B cells from normal controls fail to increase HIV production unless they are stimulated in vitro. Thus, the spontaneous production of IL-6 and TNF-alpha by B cells from individuals infected with HIV may contribute to viral expression as well as to the hypergammaglobulinemia often associated with HIV infection.