Georgoulias V, Triebel F, Kosmatopoulos C, Allouche M, Gluckman J C, Mathe G, Jasmin C
Leuk Res. 1986;10(4):419-27. doi: 10.1016/0145-2126(86)90072-x.
Peripheral blood T colony-forming cells (T-CFC) from patients with T-cell malignancies are capable of proliferation in methylcellulose, in the absence of added growth factors or mitogenic stimulation. We show here that based on the spontaneous plating efficiencies of their T-CFC, two groups of patients can be established: Group A (10 patients) with a high colony number (more than 100 colonies/10(5) seeded cells), and group B (12 patients) with less than 100 colonies/10(5) cells. The addition of interleukin 2-(IL2) containing PHA-leukocyte conditioned medium enhanced colony growth from group B but not group A patients. Moreover, both biochemically purified and recombinant IL2 induced the colony growth from group B but not group A patients without any other stimulation. In addition, a monoclonal antibody (moAb) against the IL2 receptor (IL2-R; anti-Tac) inhibited the spontaneous colony formation from T-CFC of both groups of patients. These observations strongly suggest that IL2-R are involved in the spontaneous colony growth of T-CFC. To determine whether IL2 is also involved in the spontaneous colony formation, media conditioned (LCM) by unstimulated leukemic cells were tested for IL2 activity. A constitutive release of IL2 was detected in LCM from only 2 out of 10 patients tested, and some of them were capable to inhibit thymidine incorporation by IL2-dependent cells cultured in the presence of highly purified IL2. However, most of these LCM contained a T-cell colony-promoting activity (TCPA) inducing colony formation from both normal resting and PHA-stimulated E+ clonogenic cells without added IL2 or mitogenic stimulation. TCPA-containing LCM induced the expression of functional IL2-R and IL2 release by normal resting lymphocytes. TCPA was constitutively released by blast-enriched cell fractions suggesting that it is released by the leukemic cells.
T细胞恶性肿瘤患者的外周血T集落形成细胞（T-CFC）在没有添加生长因子或丝裂原刺激的情况下，能够在甲基纤维素中增殖。我们在此表明，根据其T-CFC的自发接种效率，可以将患者分为两组：A组（10例患者）集落数高（每10⁵接种细胞超过100个集落），B组（12例患者）每10⁵细胞集落数少于100个。添加含白细胞介素2（IL2）的PHA-白细胞条件培养基可增强B组患者的集落生长，但对A组患者无效。此外，经生化纯化的IL2和重组IL2均可在无任何其他刺激的情况下诱导B组患者而非A组患者的集落生长。此外，一种针对IL2受体（IL2-R；抗Tac）的单克隆抗体可抑制两组患者T-CFC的自发集落形成。这些观察结果强烈表明，IL2-R参与了T-CFC的自发集落生长。为了确定IL2是否也参与自发集落形成，检测了未刺激的白血病细胞条件培养基（LCM）的IL2活性。在10例受试患者中，仅2例的LCM中检测到IL2的组成性释放，其中一些能够抑制在高纯度IL2存在下培养的IL2依赖性细胞的胸苷掺入。然而，这些LCM中的大多数含有T细胞集落促进活性（TCPA），可在不添加IL2或丝裂原刺激的情况下，诱导正常静息和PHA刺激的E⁺克隆形成细胞形成集落。含TCPA的LCM可诱导正常静息淋巴细胞表达功能性IL2-R并释放IL2。富含母细胞的细胞组分可组成性释放TCPA，提示它是由白血病细胞释放的。
