Tanaka Yuji, Takahashi Tsuyoshi, Nieda Mie, Masuda Shigeo, Kashiwase Koichi, Takahashi Tokiharu, Ogawa Seishi, Chiba Shigeru, Juji Takeo, Hirai Hisamaru
Department of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-8655, Japan.
Leuk Res. 2002 Mar;26(3):317-21. doi: 10.1016/s0145-2126(01)00119-9.
In the majority of Ph+ALL patients, p190 bcr-abl fusion protein is generated in the Philadelphia chromosome. The fusion protein may serve as a leukemia antigen because it is not expressed in normal cells and hardly in any other malignancy. From a healthy donor, we have established a p190 bcr-abl fusion peptide-specific CD4+ cytotoxic T-cell clone, activation of which depends on HLA-DRB1*1501. This T-cell clone has a strong cytotoxic activity against autologus MoDCs pulsed with e1a2 peptide and its cytotoxicity is not mediated by Fas/Fas ligand or perforin pathway. Success in establishment of the p190 bcr-abl fusion peptide-specific T-cell clone encourages us to develop a new approach to an effective immunotherapy for Ph+ALL.
在大多数Ph+急性淋巴细胞白血病(ALL)患者中,费城染色体产生p190 bcr-abl融合蛋白。该融合蛋白可作为白血病抗原,因为它在正常细胞中不表达,在任何其他恶性肿瘤中也几乎不表达。我们从一名健康供体中建立了一个p190 bcr-abl融合肽特异性CD4+细胞毒性T细胞克隆,其激活依赖于HLA-DRB1*1501。该T细胞克隆对用e1a2肽脉冲处理的自体单核细胞衍生树突状细胞(MoDCs)具有强大的细胞毒性活性,且其细胞毒性不是由Fas/Fas配体或穿孔素途径介导的。成功建立p190 bcr-abl融合肽特异性T细胞克隆鼓励我们开发一种针对Ph+ALL的有效免疫治疗新方法。