Orosz C G, Zinn N E, Olsen R G, Mathes L E
J Immunol. 1985 Jul;135(1):583-90.
Murine splenocytes and cloned murine T cells were used to study the in vitro immunosuppressive effects of UV-inactivated feline leukemia virus (FeLV-UV) on lymphokine secretion. FeLV-UV can significantly depress the accumulation of IL 2 in cultures of Con A-stimulated C57BL/6 splenocytes and in cultures containing the alloreactive helper T cell clone B6D/2-2m plus Con A. Inhibition of lymphokine accumulation in these cultures could not be attributed to absorption or inactivation of IL 2 by the FeLV-UV or to the FeLV-UV-induced production of substances which interfere with the IL 2 bioassay. Thus, FeLV-UV appears to block production and/or secretion of IL 2 by a direct inhibitory effect on IL 2-secreting murine T lymphocytes. Additional studies indicate that FeLV-UV impairs IL 2 production only if added very soon after lymphocyte contact with lymphokine-inducing agents and that IL 2 secretion resumes when FeLV-UV is removed from the culture. FeLV-UV also impairs accumulation of MAF (interferon-gamma?) in cultures of Con A-stimulated C57BL/6 splenocytes and in cultures containing the alloreactive cytotoxic T lymphocyte clone B6D/2-7c plus Con A. The latter observation again suggests that FeLV-UV impairs lymphokine secretion by a direct effect on lymphokine-producing T lymphocytes. Furthermore, it suggests that FeLV-UV does not selectively impair production of IL 2 nor does it have selective inhibitory effects on helper T cells. Rather, FeLV-UV appears to have a general inhibitory effect on lymphokine production by T lymphocytes. Finally, concentrations of FeLV-UV which suppress MAF production by the CTL clone have little influence on the cytolysis mediated by the same cloned T cell population. Thus, the immunosuppressive influence of FeLV-UV is selective for phenomena associated with induction of new T lymphocyte functions, such as lymphokine secretion, and spares other immune functions already expressed by the same cells.
利用小鼠脾细胞和克隆的小鼠T细胞研究紫外线灭活的猫白血病病毒(FeLV-UV)对淋巴因子分泌的体外免疫抑制作用。FeLV-UV可显著抑制在刀豆蛋白A刺激的C57BL/6脾细胞培养物中以及含有同种异体反应性辅助性T细胞克隆B6D/2-2m加刀豆蛋白A的培养物中白细胞介素2(IL 2)的积累。在这些培养物中淋巴因子积累的抑制不能归因于FeLV-UV对IL 2的吸收或灭活,也不能归因于FeLV-UV诱导产生干扰IL 2生物测定的物质。因此,FeLV-UV似乎通过对分泌IL 2的小鼠T淋巴细胞的直接抑制作用来阻断IL 2的产生和/或分泌。进一步的研究表明,只有在淋巴细胞与淋巴因子诱导剂接触后很快添加FeLV-UV,它才会损害IL 2的产生,并且当从培养物中去除FeLV-UV时,IL 2分泌会恢复。FeLV-UV还会损害在刀豆蛋白A刺激的C57BL/6脾细胞培养物中以及含有同种异体反应性细胞毒性T淋巴细胞克隆B6D/2-7c加刀豆蛋白A的培养物中巨噬细胞活化因子(MAF,干扰素-γ?)的积累。后一观察结果再次表明,FeLV-UV通过对产生淋巴因子 的T淋巴细胞的直接作用来损害淋巴因子分泌。此外,这表明FeLV-UV不会选择性地损害IL 2的产生,也不会对辅助性T细胞有选择性抑制作用。相反,FeLV-UV似乎对T淋巴细胞产生淋巴因子具有普遍抑制作用。最后,抑制细胞毒性T淋巴细胞克隆产生MAF的FeLV-UV浓度对同一克隆T细胞群体介导的细胞溶解影响很小。因此,FeLV-UV的免疫抑制作用对与诱导新的T淋巴细胞功能(如淋巴因子分泌)相关的现象具有选择性,并使同一细胞已经表达的其他免疫功能不受影响。