Shindo T, Sugie K, Nakamura K, Tagaya Y, Maeda M, Uchiyama T, Sagawa K, Yokoyama M, Wada H, Hitomi S
Institute for Immunology, Faculty of Medicine, Kyoto University, Japan.
Immunology. 1990 Sep;71(1):63-9.
Using KOLT-2 monoclonal antibody (mAb) recognizing a 44,000 molecular weight (MW) T-cell activation antigen (CD28), we observed the co-expression of KOLT-2 (CD28) antigen and Tac (CD25) antigen, associated with a 55,000 MW chain of the interleukin-2 receptor (IL-2R) complex. IL-2R (p55), on several T-cell lines transformed by human T-lymphotropic virus-I (HTLV-I), as well as several subclones of the natural killer (NK)-like cell line YT. When YT cells (YTC3T, YT5.1) and IL-2-dependent HTLV-I+ T-cell line cells (ED, ATL35C) expressing both IL-2R (p55) and IL-2R (p70) chains were cultured with recombinant IL-2 (rIL-2), KOLT-2 antigen was down-regulated in 24 hr. However, KOLT-2 antigen on HPB-ALL (Kurume) cells expressing neither of the IL-2R chains was unaffected by IL-2. IL-2 also failed to down-regulate KOLT-2 antigen on MT-1 cells bearing IL-2R (p55)/Tac without IL-2R (p70). To clarify the role of IL-2R (p70) in the IL-2-induced down-regulation of KOLT-2 antigen, we analysed the effect of IL-2 on a Tac- subclone of YT (YT2C2) that expresses IL-2R (p70). As was the case with Tac+ YT cells, KOLT-2 antigen was down-regulated by IL-2, and this down-regulation was inhibited by anti-IL-2R (p70) mAb but not by anti-Tac mAb. These results show that the signalling through the IL-2/IL-2R system down-regulates KOLT-2 (CD28) antigen by way of the interaction between IL-2 and IL-2R (p70), irrespective of IL-2R (p55)/Tac. Possible involvement of the IL-2/IL-2R system in the CD28-mediated mitogenic mechanism is discussed.
利用识别分子量为44,000的T细胞活化抗原（CD28）的KOLT-2单克隆抗体（mAb），我们观察到KOLT-2（CD28）抗原与白细胞介素-2受体（IL-2R）复合物的55,000分子量链相关的Tac（CD25）抗原的共表达。在几种由人类嗜T淋巴细胞病毒-I（HTLV-I）转化的T细胞系以及自然杀伤（NK）样细胞系YT的几个亚克隆上均检测到IL-2R（p55）。当表达IL-2R（p55）和IL-2R（p70）链的YT细胞（YTC3T、YT5.1）和IL-2依赖的HTLV-I + T细胞系细胞（ED、ATL35C）用重组IL-2（rIL-2）培养时，KOLT-2抗原在24小时内被下调。然而，在既不表达IL-2R链的HPB-ALL（久留米）细胞上，KOLT-2抗原不受IL-2影响。IL-2也未能下调携带IL-2R（p55）/Tac但不携带IL-2R（p70）的MT-1细胞上的KOLT-2抗原。为了阐明IL-2R（p70）在IL-2诱导的KOLT-2抗原下调中的作用，我们分析了IL-2对表达IL-2R（p70）的YT的Tac - 亚克隆（YT2C2）的影响。与Tac + YT细胞情况相同，KOLT-2抗原被IL-2下调，并且这种下调被抗IL-2R（p70）mAb抑制，但不被抗Tac mAb抑制。这些结果表明，通过IL-2/IL-2R系统的信号传导通过IL-2与IL-2R（p70）之间的相互作用下调KOLT-2（CD28）抗原，而与IL-2R（p55）/Tac无关。讨论了IL-2/IL-2R系统可能参与CD28介导的促有丝分裂机制。
