Lotem J, Sachs L
Department of Genetics, Weizmann Institute of Science, Rehovot, Israel.
Int J Cancer. 1987 Oct 15;40(4):532-9. doi: 10.1002/ijc.2910400417.
The normal myeloid hematopoietic regulatory proteins include 4 different growth-inducing proteins (IL-3, MGI-1GM = GM-CSF, MGI-1G = G-CSF, and MGI-1M = M-CSF = CSF-1). There is also another type of normal myeloid regulatory protein (MGI-2) with no MGI-1 (CSF or IL-3) activity, which can induce differentiation of normal myeloid precursors and certain clones of myeloid leukemic cells. Studies on the binding of MGI-2 to differentiation-competent (D+) and differentiation-defective (D-) clones of mouse myeloid leukemic cells and to normal cells indicate that: (1) D+ clones of myeloid leukemic cells had about 2,500 high-affinity surface receptors per cell, like mature normal myeloid cells, and the bound MGI-2 was rapidly internalized with its cell-surface receptors at 37 degrees C causing down-regulation of MGI-2 receptors in both the normal and leukemic cells; (2) in some D- clones, the number and internalization of MGI-2 receptors were similar to those of D+ clones whereas other D- clones had only 0-100 MGI-2 receptors per cell; (3) normal thymus and lymph-node lymphocytes and T lymphoma cells did not show detectable MGI-2 receptors; (4) there was an independent expression of receptors for MGI-2 and for the 4 myeloid growth-inducing proteins on different clones of myeloid leukemic cells; and (5) none of the 4 myeloid growth-inducing proteins IL-3, MGI-1GM, MGI-1G, or MGI-1M, inhibited binding of MGI-2 to its receptors. The cytotoxic proteins lymphotoxin and tumor necrosis factor did not induce differentiation of the mouse myeloid leukemic cells and also did not inhibit binding of MGI-2 to its receptors. These results show that the myeloid differentiation-inducing protein MGI-2 binds to cell-surface receptors that are different from the receptors for the 4 myeloid growth-inducing proteins and these cytotoxic proteins.
正常髓系造血调节蛋白包括4种不同的生长诱导蛋白（白细胞介素-3、MGI-1GM = 粒细胞-巨噬细胞集落刺激因子、MGI-1G = 粒细胞集落刺激因子、MGI-1M = 巨噬细胞集落刺激因子 = 集落刺激因子-1）。还有另一种正常髓系调节蛋白（MGI-2），它没有MGI-1（集落刺激因子或白细胞介素-3）活性，可诱导正常髓系前体细胞和某些髓系白血病细胞克隆的分化。对MGI-2与小鼠髓系白血病细胞的分化能力正常（D+）和分化缺陷（D-）克隆以及正常细胞的结合研究表明：（1）髓系白血病细胞的D+克隆每个细胞约有2500个高亲和力表面受体，与成熟正常髓系细胞一样，在37℃时，结合的MGI-2与其细胞表面受体一起迅速内化，导致正常细胞和白血病细胞中MGI-2受体下调；（2）在一些D-克隆中，MGI-2受体的数量和内化情况与D+克隆相似，而其他D-克隆每个细胞只有0 - 100个MGI-2受体；（3）正常胸腺和淋巴结淋巴细胞以及T淋巴瘤细胞未显示可检测到的MGI-2受体；（4）在髓系白血病细胞的不同克隆上，MGI-2受体与4种髓系生长诱导蛋白的受体独立表达；（5）4种髓系生长诱导蛋白白细胞介素-3、MGI-1GM、MGI-1G或MGI-1M均不抑制MGI-2与其受体的结合。细胞毒性蛋白淋巴毒素和肿瘤坏死因子不诱导小鼠髓系白血病细胞分化，也不抑制MGI-2与其受体的结合。这些结果表明，髓系分化诱导蛋白MGI-2与不同于4种髓系生长诱导蛋白和这些细胞毒性蛋白的受体的细胞表面受体结合。
