THE P75 PEPTIDE IS THE RECEPTOR FOR INTERLEUKIN-2 EXPRESSED ON LARGE ANTIGRANULOCYTES LYMPHOCYTES AND IS RESPONSIBLE FOR THE INTERLEUKIN-2 ACTIVATION OF THESE CELLS
THE P75 PEPTIDE IS THE RECEPTOR FOR INTERLEUKIN-2 EXPRESSED ON LARGE ANTIGRANULOCYTES LYMPHOCYTES AND IS RESPONSIBLE FOR THE INTERLEUKIN-2 ACTIVATION OF THESE CELLS
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DOI：
10.1073/pnas.84.15.5394
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发表时间：
1987-08-01
影响因子：
11.1
通讯作者：
WALDMANN, TA
中科院分区：
文献类型：
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作者：
TSUDO, M;GOLDMAN, CK;WALDMANN, TA
白细胞介素2 （IL-2）结合肽至少有两种：一种是与抗tac单克隆抗体反应的Mr为55,000的肽（p55），另一种是Mr为75,000的非tac IL-2结合肽（p75）。独立存在的Tac或p75肽代表低亲和力的IL-2受体，而高亲和力的IL-2受体则在这两种肽存在并与受体复合物相关时表达。人们早就知道，来自LGL异常扩增患者的正常大颗粒淋巴细胞（LGL）或白血病细胞不仅可以被IL-2激活为更强效的自然杀伤细胞，而且还可以被激活为淋巴因子激活杀伤细胞（LAK）活性的效应器，尽管它们不表达Tac肽。在本研究中，使用交联方法，我们发现所有被测试个体的正常LGL和白血病LGL表达p75 IL-2结合肽，但不表达Tac肽。这些LGL白血病细胞对IL-2有增殖反应，但需要比表达高亲和力受体的正常植物血凝素刺激的T淋巴细胞增殖所需的浓度高得多。此外，在Tac阴性的LGL白血病细胞中添加IL-2可增强Tac基因的转录并诱导Tac肽。il -2诱导的细胞增殖和Tac基因的表达不受抗Tac的抑制。这些结果有力地表明p75肽负责il -2诱导的LGL激活，p75肽可能在il -2介导的免疫应答中发挥重要作用，不仅通过与Tac肽一起参与T细胞上高亲和力受体复合物的形成，而且还有助于初始触发LGL激活，使这些细胞成为有效的自然杀手和淋巴因子激活的杀手细胞。
There are at least two interleukin 2 (IL-2) binding peptides: one is the Mr 55,000 peptide (p55) reactive with the anti-Tac monoclonal antibody, and the other is a Mr 75,000 non-Tac IL-2 binding peptide (p75). Independently existing Tac or p75 peptides represent low-affinity IL-2 receptors, whereas high-affinity IL-2 receptors are expressed when both peptides are present and associated in a receptor complex. It has long been known that normal large granular lymphocytes (LGL) or leukemic cells from the patients with abnormal expansions of LGL can be activated by IL-2 not only to more-potent natural killer cells but also to effectors of lymphokine-activated killer (LAK) activity, although they do not express the Tac peptide. In the present study, using cross-linking methodology, we found that normal LGL and leukemic LGL from all individuals tested expressed the p75 IL-2 binding peptide but did not express the Tac peptide. These LGL leukemia cells made proliferative responses to IL-2 but required a much higher concentration than that required for the proliferation of normal phytohemagglutinin-stimulated T lymphoblasts that express high-affinity receptors. Furthermore, the addition of IL-2 to Tac-negative LGL leukemic cells augmented transcription of the Tac gene and induced the Tac peptide. Neither the IL-2-induced proliferation nor the unregulation of Tac gene expression was inhibited by the addition of anti-Tac. These results strongly suggest that the p75 peptide is responsible for IL-2-induced activation of LGL and that the p75 peptide may play an important role in the IL-2-mediated immune response not only by participating with the Tac peptide in the formation of the high-affinity receptor complex on T cells but also by contributing to the initial triggering of LGL activation so that these cells become efficient natural killer and lymphokine-activated killer cells.