Brooks K H, Vitetta E S
J Immunol. 1986 Nov 15;137(10):3205-10.
We have used a lymphokine-responsive clone (3B3) of B leukemia cells (BCL1) to examine the effects of several recombinant and purified lymphokines. Cells from BCL1-3B3 were induced to secrete IgM in the presence of recombinant interleukin 2 (rIL 2) (10 to 50 U/ml); a concomitant increase in proliferation was observed. Recombinant interferon-gamma (rIFN-gamma) was a potent inhibitor of proliferation. In addition, rIFN-gamma did not induce an increase in IgM secretion and, when added to rIL 2-stimulated BCL1-3B3 cells, completely blocked IgM secretion at a concentration of 10 U/ml. Purified and recombinant IL 1 (rIL 1) had no significant effect on differentiation either alone or in combination with rIL 2 and/or rIFN-gamma. However, rIL 1 was able to synergize with rIL 2 in enhancing the proliferation of BCL1-3B3. The ability of cells to respond to rIL 2 was limited to the in vitro (Ly-1+) clones of BCL1 cells since the in vivo derived (Ly-1-) BCL1 cells did not differentiate in response to IL 2. Consistent with their functional response to rIL 2, cells from the in vitro clone (3B3) are IL 2-receptor-positive (IL-2R+) and the in vivo derived BCL1 cells are IL-2R-. A second set of neoplastic B cell clones derived from the AKR 225 lymphoma did not respond to rIL 2 even though they expressed receptors for IL 2 and could be induced by T cell supernatant to secrete IgM, thus indicating that expression of IL 2R is not the sole requirement for IL 2 responsiveness. The monoclonal anti-IL 2R antibody (7D4) mimicked IL 2 in its ability to stimulate differentiation of BCL1-3B3 cells. These data suggest that rIL 2 and the monoclonal anti-IL-2R antibody are capable of inducing a differentiative response in the Ly-1+ BCL1-3B3 cells that is functionally equivalent to the response evoked by the previously described lymphokine B cell differentiation factor for IgM (BCDF mu). Thus, two distinct lymphokines appear to be providing a similar signal to a clonal neoplastic B cell population. Furthermore, rIL 2 is capable of providing both a proliferative and a differentiative signal.
我们使用了B淋巴细胞白血病细胞（BCL1）的一个淋巴因子反应性克隆（3B3）来检测几种重组和纯化淋巴因子的作用。在重组白细胞介素2（rIL 2）（10至50 U/ml）存在的情况下，来自BCL1 - 3B3的细胞被诱导分泌IgM；同时观察到增殖增加。重组干扰素 - γ（rIFN - γ）是一种有效的增殖抑制剂。此外，rIFN - γ不会诱导IgM分泌增加，并且当添加到rIL 2刺激的BCL1 - 3B3细胞中时，在浓度为10 U/ml时完全阻断IgM分泌。纯化的和重组的白细胞介素1（rIL 1）单独或与rIL 2和/或rIFN - γ联合使用时对分化均无显著影响。然而，rIL 1能够与rIL 2协同增强BCL1 - 3B3的增殖。细胞对rIL 2的反应能力仅限于BCL1细胞的体外（Ly - 1 +）克隆，因为体内来源的（Ly - 1 -）BCL1细胞对IL 2无反应。与它们对rIL 2的功能反应一致，来自体外克隆（3B3）的细胞是白细胞介素2受体阳性（IL - 2R +），而体内来源的BCL1细胞是IL - 2R -。另一组源自AKR 225淋巴瘤的肿瘤性B细胞克隆对rIL 2无反应，尽管它们表达白细胞介素2受体并且可以被T细胞上清液诱导分泌IgM，因此表明白细胞介素2受体的表达不是对白细胞介素2反应性的唯一要求。单克隆抗白细胞介素2受体抗体（7D4）在刺激BCL1 - 3B3细胞分化的能力上模拟了白细胞介素2。这些数据表明，rIL 2和单克隆抗白细胞介素2受体抗体能够在Ly - 1 + BCL1 - 3B3细胞中诱导一种分化反应，该反应在功能上等同于先前描述的淋巴因子B细胞IgM分化因子（BCDFμ）所引发的反应。因此，两种不同的淋巴因子似乎正在向一个克隆性肿瘤性B细胞群体提供类似的信号。此外，rIL 2能够提供增殖和分化信号。
