Burdach S E, Levitt L J
Blood. 1987 May;69(5):1368-75.
Interleukin-2 (IL-2) induces differential secretion of lymphokines by IL-2 receptor (IL-2R)-positive and IL-2R-negative T cells. We studied T cell IL-2R-specific modulation of adult bone marrow erythropoiesis by recombinant IL-2 (rIL-2). I3-2R were induced by CD3 T cell surface determinant-triggering and analyzed by cytofluorography. Bone marrow monocyte and T cell-depleted (NAB-T) target cells were assessed for early erythroid progenitor expression (BFU-E) in the presence of 0 to 10(3) U/mL of rIL-2, rIL-2 had no significant effect on BFU-E expression in the absence of T cells or in the presence of IL-2R-negative T cells. rIL-2 caused a dose-dependent inhibition (75% to 90%) of BFU-E in the presence of autologous IL-2R-positive T cells. The addition of anti-IL2-receptor antibody to cultures containing rIL-2 plus IL-2R-positive T cells entirely abrogated rIL-2-mediated inhibition of BFU-E. In the presence of rIL-2 (10(2) U/mL) production of interferon gamma (IF-gamma) by adult marrow CD3-triggered IL-2R-positive T cells was increased 37- to 125-fold compared to IL-2R-negative T cells. rIF-gamma caused a dose-dependent (88% +/- 17% at 10(3) U/mL) inhibition of adult BFU-E in the presence of CD3-triggered autologous T cells. rIL2-mediated inhibition of adult BFU-E in the presence of IL-2R-positive T cells was partially abrogated (52% +/- 16%) following addition of monospecific IF-gamma antibody. These results demonstrate (a) rIL-2 modulation of adult marrow erythropoiesis is selectively dependent upon both the presence or absence of autologous T cells and the IL-2R status of these T cells; and (b) rIL-2-induced inhibition of adult marrow erythropoiesis is mediated in part by release of IF-gamma from IL-2R-positive T cells.
白细胞介素-2（IL-2）可诱导白细胞介素-2受体（IL-2R）阳性和IL-2R阴性T细胞分泌不同的淋巴因子。我们研究了重组IL-2（rIL-2）对成年骨髓红细胞生成的T细胞IL-2R特异性调节作用。通过CD3 T细胞表面决定簇触发诱导IL-2R，并通过细胞荧光术进行分析。在存在0至10³ U/mL rIL-2的情况下，评估骨髓单核细胞和T细胞耗尽的（NAB-T）靶细胞的早期红系祖细胞表达（BFU-E）。在没有T细胞或存在IL-2R阴性T细胞的情况下，rIL-2对BFU-E表达没有显著影响。在存在自体IL-2R阳性T细胞的情况下，rIL-2导致BFU-E呈剂量依赖性抑制（75%至90%）。向含有rIL-2加IL-2R阳性T细胞的培养物中添加抗IL-2受体抗体完全消除了rIL-2介导的对BFU-E的抑制作用。与IL-2R阴性T细胞相比，在rIL-2（10² U/mL）存在的情况下，成年骨髓CD3触发的IL-2R阳性T细胞产生的干扰素γ（IF-γ）增加了37至125倍。在存在CD3触发的自体T细胞的情况下，rIF-γ导致成年BFU-E呈剂量依赖性抑制（在10³ U/mL时为88%±17%）。添加单特异性IF-γ抗体后，在存在IL-2R阳性T细胞的情况下，rIL-2介导的对成年BFU-E的抑制作用部分被消除（52%±16%）。这些结果表明：（a）rIL-2对成年骨髓红细胞生成的调节选择性地依赖于自体T细胞的存在与否以及这些T细胞的IL-2R状态；（b）rIL-2诱导的对成年骨髓红细胞生成的抑制部分是由IL-2R阳性T细胞释放IF-γ介导的。
