Moreau J F, Bonneville M, Peyrat M A, Jacques Y, Soulillou J P
Ann Inst Pasteur Immunol (1985). 1986 Jan-Feb;137C(1):25-37. doi: 10.1016/s0771-050x(86)80003-1.
Several T-lymphocyte clones obtained from rejected human kidney allografts and maintained for several months in recombinant IL2 and antigen-supplemented cultures were studied for their capacity to produce lymphokines in vitro. Six clones produced a factor able to increase 3HTdR uptake of the IL3-dependent DA-1 murine cell line. All were T4+, T3+ and T11+ and fitted with a probability of monoclonality above 97%. The factor, designated as human-interleukin-DA (HILDA), was not produced when autologous EBV-transformed B cells were added in the culture in the absence of exogenous IL2. Addition of pure recombinant IL2 along with donor EBV-transformed cell lines resulted in a sharp increase in HILDA yield, whereas a low amount of this factor was also produced with the autologous EBV B lymphocyte in the presence of exogenous IL2. Kinetics studies show that HILDA was detectable as early as 24 to 48 h, peaked at day 3 and plateaued until day 5. The antigen-exogenous IL2-driven pathway of HILDA production by clones was bypassed by use of either PMA or calcium ionophore (CaI) alone or associated in the culture. Both compounds induced dose-related HILDA production (without antigen and/or exogenous IL2). No synergistic effect of PMA and CaI was noted, although an additional effect could be seen when a suboptimal dose of CaI was used.
从被排斥的人肾同种异体移植物中获得并在重组白细胞介素2（IL2）和添加抗原的培养物中维持数月的几个T淋巴细胞克隆，对其体外产生淋巴因子的能力进行了研究。六个克隆产生了一种能够增加IL3依赖的DA-1鼠细胞系3HTdR摄取的因子。所有克隆均为T4+、T3+和T11+，单克隆性概率超过97%。该因子被命名为人白细胞介素-DA（HILDA），当在无外源性IL2的培养物中加入自体EB病毒转化的B细胞时不产生。加入纯重组IL2以及供体EB病毒转化的细胞系会导致HILDA产量急剧增加，而在外源性IL2存在的情况下，自体EB病毒B淋巴细胞也会产生少量这种因子。动力学研究表明，最早在24至48小时可检测到HILDA，在第3天达到峰值，并持续到第5天保持稳定。通过在培养中单独使用佛波酯（PMA）或钙离子载体（CaI）或两者联合使用，绕过了克隆产生HILDA的抗原-外源性IL2驱动途径。两种化合物均诱导与剂量相关的HILDA产生（无抗原和/或外源性IL2）。未观察到PMA和CaI的协同作用，尽管当使用次优剂量的CaI时可看到额外的效应。
