Miedema F, Van Oostveen J W, Sauerwein R W, Terpstra F G, Aarden L A, Melief C J
Eur J Immunol. 1985 Feb;15(2):107-12. doi: 10.1002/eji.1830150202.
The role of interleukin 2 (IL2) in the induction of human B cell differentiation in vitro was studied. IL2 was unable to induce immunoglobulin (Ig) production in non-T cells either in the presence or absence of pokeweed mitogen (PWM). However, IL2 alone could induce Ig production in non-T cells when irradiated T cells were present. Similar to the PWM-driven system helper activity was delivered by T4+ but not T8+ cells. Apparently, IL2 acts on T4+ cells and induces these cells to deliver the actual helper signal(s) for Ig production by B cells. Whereas in the PWM-driven system only T8+ cells suppress Ig synthesis, IL2-driven Ig synthesis was suppressed by both T4+ and T8+ cells added to a mixture of non-T cells and irradiated T4+ cells. This suppressor activity could be abrogated by irradiation. PWM was shown to induce IL2 production in both T4+ and T8+ cells. Moreover, PWM-induced Ig synthesis, like IL2-induced Ig synthesis, could be totally abrogated by a monoclonal antibody against the human IL2 receptor (anti-Tac). These findings, coupled to the innate Ig-inducing capacity of IL2, indicate a role for IL2 in the PWM-driven system. The mechanism of suppression in both the PWM- and the IL2-driven systems was not shortage of IL2 in the culture due to consumption or inhibition of production of IL2. Moreover, the T8+ cells produced IL2, despite their failure to help Ig synthesis. Helper T cell activity can thus be divided into two distinct activities: IL2 production and the ability to deliver the actual helper signal such as helper factors for B cell differentiation. This insight allows a better evaluation of the immunoregulatory activities of T cell subsets in health and disease.
研究了白细胞介素2(IL2)在体外诱导人B细胞分化中的作用。无论有无商陆有丝分裂原(PWM),IL2均无法在非T细胞中诱导免疫球蛋白(Ig)产生。然而,当存在经辐照的T细胞时,单独的IL2可在非T细胞中诱导Ig产生。与PWM驱动系统类似,辅助活性由T4 +细胞而非T8 +细胞提供。显然,IL2作用于T4 +细胞,并诱导这些细胞传递B细胞产生Ig的实际辅助信号。在PWM驱动系统中,只有T8 +细胞抑制Ig合成,而在非T细胞与经辐照的T4 +细胞的混合物中加入T4 +和T8 +细胞均可抑制IL2驱动的Ig合成。这种抑制活性可通过辐照消除。已证明PWM可诱导T4 +和T8 +细胞产生IL2。此外,PWM诱导的Ig合成,如IL2诱导的Ig合成,可被抗人IL2受体单克隆抗体(抗Tac)完全消除。这些发现,再加上IL2固有的Ig诱导能力,表明IL2在PWM驱动系统中发挥作用。PWM和IL2驱动系统中的抑制机制并非由于IL2的消耗或产生抑制导致培养物中IL2短缺。此外,T8 +细胞产生IL2,尽管它们无法促进Ig合成。因此,辅助性T细胞活性可分为两种不同的活性:IL2产生以及传递实际辅助信号(如B细胞分化辅助因子)的能力。这一见解有助于更好地评估健康和疾病状态下T细胞亚群的免疫调节活性。