Blotta M H, Marshall J D, DeKruyff R H, Umetsu D T
Department of Pediatrics, Stanford University, CA 94305, USA.
J Immunol. 1996 May 1;156(9):3133-40.
Although there is good evidence that the induction of IL-4 synthesis in CD4+ T lymphocytes is favored by Ag presentation by B cells and not macrophages, the precise molecular signals provided by B cells to T cells that enhance IL-4 synthesis are not clear. To examine this issue, we established an APC-independent system to activate highly purified T cells and induce cytokine synthesis, using immobilized mAbs against several T cell surface molecules, including CD3, CD28, and the CD40 ligand (CD40L). The counter-receptors for all three of these molecules are expressed on B cells, and include CD40, which is expressed primarily on B cells, but also on dendritic cells and thymic epithelium. We found that IL-4 synthesis was greatly enhanced by triggering of CD40L on the T cell surface in conjunction with ligation of CD3/TCR and CD28, whereas ligation of CD3/TCR and CD28 in the absence of CD40L triggering resulted in little or no IL-4 synthesis. CD40L costimulation greatly enhanced IL-4 synthesis both in T cells from normal nonallergic adult subjects as well as in naive T cells from cord blood. Furthermore, we demonstrated that IL-4 synthesis was optimally enhanced when the strength of the CD3/TCR signal was limiting, while IL-4 synthesis was inhibited when CD3/TCR stimulation was maximal. These studies confirm that IL-4 synthesis can be induced in normal T lymphocytes in the absence of exogenous IL-4, and demonstrate that CD40L costimulation is of fundamental importance in regulation of IL-4 production. In addition, these findings provide a mechanism by which B cells preferentially enhance IL-4 synthesis in T cells at low Ag concentrations.
尽管有充分证据表明,CD4+ T淋巴细胞中IL-4合成的诱导更倾向于由B细胞而非巨噬细胞进行抗原呈递,但B细胞向T细胞提供的增强IL-4合成的确切分子信号尚不清楚。为研究此问题,我们建立了一个不依赖抗原呈递细胞(APC)的系统来激活高度纯化的T细胞并诱导细胞因子合成,该系统使用针对几种T细胞表面分子(包括CD3、CD28和CD40配体(CD40L))的固定化单克隆抗体。这三种分子的对应受体均在B细胞上表达,包括主要在B细胞上表达,但也在树突状细胞和胸腺上皮细胞上表达的CD40。我们发现,T细胞表面CD40L的触发与CD3/TCR和CD28的连接相结合可极大地增强IL-4合成,而在没有CD40L触发的情况下连接CD3/TCR和CD28则几乎不会导致IL-4合成。CD40L共刺激在来自正常非过敏成年受试者的T细胞以及来自脐带血的初始T细胞中均极大地增强了IL-4合成。此外,我们证明当CD3/TCR信号强度有限时,IL-4合成得到最佳增强,而当CD3/TCR刺激最大时,IL-4合成受到抑制。这些研究证实,在没有外源性IL-4的情况下,正常T淋巴细胞中可诱导IL-4合成,并表明CD40L共刺激在IL-4产生的调节中至关重要。此外,这些发现提供了一种机制,通过该机制B细胞在低抗原浓度下优先增强T细胞中的IL-4合成。