Hsu S M, Tseng C K, Hsu P L
Department of Pathology, University of Texas, Houston 77225.
Am J Pathol. 1990 Apr;136(4):735-44.
The authors studied the secretion of interleukin-2 (IL-2), the expression of interleukin-2 receptors (IL-2R; p55/Tac and p75), and the response to exogenous IL-2 by cultured Hodgkin's Reed-Sternberg cells (cell lines HDLM-1, HDLM-1d, and KM-H2) and T cells (H9, HuT78, HuT102, MOLT-4, and MT-2). All of these cells did not produce IL-2 or produced it in undetectable amounts, and their growth was not affected by the addition of anti-IL-2 or anti-IL-2R antibodies. This indicates that H-RS cells in long-term culture, as well as T cells, can grow independently of IL-2. The three H-RS cell lines, as well as two of the T-cell lines (HuT102 and MT-2), expressed Tac, whereas the other three T-cell lines were Tac negative. Expression of p75 was noted in the two Tac-positive T-cell lines, but not in cultured H-RS cells. The expression of Tac and p75 in HuT102 and MT-2 cells correlated well with their capacity to proliferate on treatment with exogenous IL-2. On IL-2 treatment, nucleic-acid uptake in Tac/p75-positive T cells increased approximately four- to sixfold, whereas the Tac/p75-negative T cells did not show increased proliferation. Unlike the T cells, the Tac-positive H-RS cells did not respond to IL-2. The lack of a proliferative response to IL-2 appears to be related to the absence of p75 in H-RS cells. A similar pattern (Tac positivity and p75 negativity) was noted in H-RS cells in lymph nodes involved by Hodgkin's disease. Thus the exogenous IL-2 released by surrounding T lymphocytes may not cause the proliferative activity of H-RS cells because of the lack of high-affinity IL-2 receptors in the latter cells. In contrast to H-RS cells in culture, H-RS cells in tissues were stained by a specific anti-IL-2 monoclonal antibody. This indicates that the expression of IL-2 or an IL-2-like substance by H-RS cells in tissues may be responsible, in part, for the great increase in the number of reactive T lymphocytes in tissues involved by Hodgkin's disease.
作者研究了白细胞介素-2(IL-2)的分泌、白细胞介素-2受体(IL-2R;p55/Tac和p75)的表达,以及培养的霍奇金里德-斯腾伯格细胞(细胞系HDLM-1、HDLM-1d和KM-H2)和T细胞(H9、HuT78、HuT102、MOLT-4和MT-2)对外源性IL-2的反应。所有这些细胞均不产生IL-2或产生量无法检测到,并且添加抗IL-2或抗IL-2R抗体对其生长没有影响。这表明长期培养的霍奇金里德-斯腾伯格细胞以及T细胞可以独立于IL-2生长。三种霍奇金里德-斯腾伯格细胞系以及两种T细胞系(HuT102和MT-2)表达Tac,而其他三种T细胞系Tac呈阴性。在两种Tac阳性T细胞系中检测到p75的表达,但在培养的霍奇金里德-斯腾伯格细胞中未检测到。HuT102和MT-2细胞中Tac和p75的表达与其用外源性IL-2处理后的增殖能力密切相关。在用IL-2处理时,Tac/p75阳性T细胞中的核酸摄取增加约四至六倍,而Tac/p75阴性T细胞未显示增殖增加。与T细胞不同,Tac阳性的霍奇金里德-斯腾伯格细胞对IL-2无反应。对IL-2缺乏增殖反应似乎与霍奇金里德-斯腾伯格细胞中缺乏p75有关。在霍奇金病累及的淋巴结中的霍奇金里德-斯腾伯格细胞中也观察到类似模式(Tac阳性和p75阴性)。因此,由于后者细胞中缺乏高亲和力IL-2受体,周围T淋巴细胞释放的外源性IL-2可能不会引起霍奇金里德-斯腾伯格细胞的增殖活性。与培养中的霍奇金里德-斯腾伯格细胞不同,组织中的霍奇金里德-斯腾伯格细胞被特异性抗IL-2单克隆抗体染色。这表明组织中的霍奇金里德-斯腾伯格细胞表达IL-2或类似IL-2的物质可能部分负责霍奇金病累及组织中反应性T淋巴细胞数量的大幅增加。