Giri J G, Kincade P W, Mizel S B
J Immunol. 1984 Jan;132(1):223-8.
In this study we have examined the effect of interleukin 1 (IL 1) on the maturation of normal and neoplastic pre-B cells. We have found that IL 1 can enhance the in vitro functional maturation of surface immunoglobulin negative (sIg-) pre-B cells from normal bone marrow. In addition, IL 1 specifically induced sIg expression on an established pre-B cell line, 70Z/3. These effects of IL 1 were obtained with the same concentrations of IL 1 that are effective in assays for T cell proliferation and functional activation. Previous studies by other investigators have demonstrated that LPS can also induce the expression of sIg on 70Z/3 cells. The stimulatory effect of LPS was dependent on the stimulation of kappa-light chain synthesis, the synthesis of mu-chains being constitutive. Our results indicate that IL 1 may also enhance sIg expression via the induction of kappa-light chain synthesis. The stimulatory effect of IL 1 was not due to contaminating LPS in the IL 1 preparations, because removal of the IL 1 by using specific antibodies against IL 1 and fixed Staphylococcus aureus cells resulted in the disappearance of kappa-chain inducing activity. In addition to IL 1, a pH 2-sensitive mediator(s) present in concanavalin A (Con A)-stimulated spleen cell supernatants was also shown to induce kappa-chain synthesis and the appearance of sIg on 70Z/3 cells. Removal of IL 1 or the inhibition of any contaminating LPS activity with polymyxin B did not diminish the activity of the pH 2-sensitive Con A supernatant factor(s). On the basis of our findings, we have concluded that IL 1 may enhance antibody responses by not only increasing the number of helper T cells but also by stimulating the maturation of B cell precursors.
在本研究中,我们检测了白细胞介素1(IL-1)对正常和肿瘤性前B细胞成熟的影响。我们发现,IL-1可增强来自正常骨髓的表面免疫球蛋白阴性(sIg-)前B细胞的体外功能成熟。此外,IL-1特异性诱导已建立的前B细胞系70Z/3上sIg的表达。IL-1的这些作用是在与T细胞增殖和功能激活检测中有效的相同浓度的IL-1下获得的。其他研究者先前的研究表明,脂多糖(LPS)也可诱导70Z/3细胞上sIg的表达。LPS的刺激作用依赖于κ轻链合成的刺激,μ链的合成是组成性的。我们的结果表明,IL-1也可能通过诱导κ轻链合成来增强sIg的表达。IL-1的刺激作用不是由于IL-1制剂中污染的LPS,因为使用抗IL-1的特异性抗体和固定的金黄色葡萄球菌细胞去除IL-1导致κ链诱导活性消失。除IL-1外,在伴刀豆球蛋白A(Con A)刺激的脾细胞上清液中存在的一种pH 2敏感介质也被证明可诱导70Z/3细胞上κ链的合成和sIg的出现。去除IL-1或用多粘菌素B抑制任何污染的LPS活性并不会降低pH 2敏感的Con A上清液因子的活性。根据我们的发现,我们得出结论,IL-1可能不仅通过增加辅助性T细胞的数量,还通过刺激B细胞前体的成熟来增强抗体反应。