Bellgrau D, Talmage D W
Proc Natl Acad Sci U S A. 1986 May;83(10):3412-6. doi: 10.1073/pnas.83.10.3412.
The thoracic duct lymphocytes from rats previously injected with ultraviolet-light-irradiated allogeneic lymphocytes were grown for 4 days with alloantigen, with or without Con A-induced lymphokine factors, and then for 3 days with the lymphokines alone. They were then tested for their cytoxicity and for their capacity to make interleukin 2 (IL-2) in response to antigen. The results show that T helper cells specific for both class I and class II antigens of the major histocompatibility complex were removed from the circulation by the injection of ultraviolet-irradiated alloantigen. However, precursors of cytotoxic cells remained and appeared to lose their OX-19 markers during activation. We have interpreted the results by using a speculative model that involves separate pathways of induction to cytotoxicity and IL-2 synthesis. We propose that the OX-19 marker is associated with the interleukin 1 receptor and that the latter is required for the IL-2 production pathway but not for activation to cytotoxicity.
将先前注射过紫外线照射的同种异体淋巴细胞的大鼠的胸导管淋巴细胞,在有或无伴刀豆球蛋白A诱导的淋巴因子的情况下,与同种抗原一起培养4天,然后仅与淋巴因子一起培养3天。然后检测它们的细胞毒性以及对抗原作出反应产生白细胞介素2(IL-2)的能力。结果表明,通过注射紫外线照射的同种抗原,从循环中清除了对主要组织相容性复合体的I类和II类抗原均具有特异性的T辅助细胞。然而,细胞毒性细胞的前体仍然存在,并且在激活过程中似乎失去了它们的OX-19标记。我们通过使用一个推测性模型来解释这些结果,该模型涉及到细胞毒性和IL-2合成的单独诱导途径。我们提出,OX-19标记与白细胞介素1受体相关联,并且后者是IL-2产生途径所必需的,但不是细胞毒性激活所必需的。