Vazquez A, Mills S, Maizel A
Roger Williams General Hospital, Department of Pathology, Providence, RI 02908.
J Immunol. 1989 Jan 1;142(1):94-9.
Several human T cell derived factors capable of stimulating human B cells to synthesize DNA have been previously described. One such factor exhibits an apparent m.w. of 50,000 Da and has been termed 50-kDa-B cell growth factor (BCGF). In this report, we show that a human B cell proliferation pathway based on the sequential action of anti-mu antibody, 50-kDa-BCGF and IL-2 is inhibited in the presence of human rIL-4. Although IL-4 itself is capable of triggering B cell DNA synthesis as measured at 72 h, this lymphokine inhibits, in a dose-related manner, the 50-kDa-BCGF driven response of B cells to IL-2 when such proliferation is determined after 144 h. This inhibition takes place at an early step of the B cell activation and does not require the presence of IL-4 during the whole culture period. Such inhibitory activity of IL-4 is specific to the IL-2-induced B cell proliferation because DNA synthesis measured in the presence of semi-purified human 12-kDa-BCGF is not affected by the presence of IL-4. Our results suggest that a particular pathway of human B cell activation leading to the proliferation of these cells in the presence of IL-2 could be either up- or down-modulated by 50-kDa-BCGF and IL-4, respectively.
先前已描述了几种能够刺激人B细胞合成DNA的人T细胞衍生因子。其中一种因子的表观分子量为50,000 Da，被称为50-kDa-B细胞生长因子（BCGF）。在本报告中，我们表明，在人rIL-4存在的情况下，基于抗μ抗体、50-kDa-BCGF和IL-2的顺序作用的人B细胞增殖途径受到抑制。尽管IL-4本身能够在72小时时触发B细胞DNA合成，但当在144小时后测定这种增殖时，这种淋巴因子以剂量相关的方式抑制B细胞对IL-2的50-kDa-BCGF驱动的反应。这种抑制发生在B细胞活化的早期阶段，并且在整个培养期间不需要IL-4的存在。IL-4的这种抑制活性对IL-2诱导的B细胞增殖具有特异性，因为在半纯化的人12-kDa-BCGF存在下测定的DNA合成不受IL-4存在的影响。我们的结果表明，在IL-2存在下导致这些细胞增殖的人B细胞活化的特定途径可能分别被50-kDa-BCGF和IL-4上调或下调。
