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目的：ＩＬ７可刺激一些良性和恶性淋巴细胞增生，其中包括来自皮肤样Ｔ细胞瘤（ＣＴＣＬ）病人的肿瘤细胞。Ｊａｎｕｓ激酶家族（ＪＡＫｓ）与许多细胞因子受体的信号传导系统有关。ＪＡＫ３是ＪＡＫｓ激酶家族的新成员，其在自然杀伤细胞（ＮＫ）和活化的Ｔ细胞上表达，并在这些细胞中从功能上和物理上与白细胞介素２受体（ＩＬ２Ｒ）结合起来。为此，本研究进一步探讨白细胞介素７（ＩＬ７）引起皮肤样Ｔ细胞瘤肿瘤细胞ＪＡＫ３的磷酸化和活化。方法：ＣＴＣＬ外周血中分离的肿瘤细胞，用ＩＬ７分别处理１、５、１０、２０ｍｉｎ，蛋白裂解物用抗ＪＡＫ３抗体，抗ｐ５９ｆｙｎ抗体进行免疫沉淀，用抗ＪＡＫ３和抗磷酸化酪氨酸作Ｗｅｓｔｅｒｎ印迹检测。结果：ＩＬ７能引起ＣＴＣＬ肿瘤细胞的ＪＡＫ３酪氨酸磷酸化，抗ｐ５９ｆｙｎ抗体能结合ＪＡＫ３，未发现ＩＬ１２能诱导ＣＴＣＬ细胞的ＪＡＫ３磷酸化。结论：提示ＩＬ７可能在ＣＴＣＬ的病理生理学上起一定的作用，且证实在ＣＴＣＬ细胞中ＩＬ７受体介导了酪氨酸磷酸化的信号传导途径。
Objective: IL 7 can stimulate some benign and malignant lymphocyte proliferation, including tumor cells from patients with skin-like T-cell tumor (CTCL). The Janus kinase family (JAKs) is involved in the signaling system of many cytokine receptors. JAK-3 is a novel member of the JAKs kinase family, which is expressed on natural killer (NK) and activated T cells and is functionally and physically associated with interleukin-2 receptors (IL-2R) in these cells. )Combined. Therefore, this study further explored that interleukin7 (IL7) causes the phosphorylation and activation of JAK3 tumor cells in skin-like T-cell neoplasms. METHODS: Tumor cells isolated from peripheral blood of CTCL were treated with IL-7 for 1, 5, 10, and 20 min, respectively. Protein lysates were anti-JAK 3 antibody, anti-p59fyn antibody was used for immunoprecipitation, and anti-JAK 3 and anti-phosphoric acid were used. The tyrosine was detected by Western blotting. Results: IL-7 can cause JAK-3 tyrosine phosphorylation in CTCL tumor cells, anti-p59fyn antibody can bind JAK-3, and IL-12 can not induce JAK-3 phosphorylation in CTCL cells. Conclusion: It is suggested that IL7 may play a role in the pathophysiology of CTCL, and it is confirmed that IL7 receptor mediates the signal transduction pathway of tyrosine phosphorylation in CTCL cells.