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目的：验证慢性粒细胞白血病（ＣＭＬ）患者体内是否存在细胞毒Ｔ淋巴细胞前体细胞，并鉴定其表型和功能特征。方法：用混合淋巴瘤细胞培养技术，用自体瘤细胞和细胞因子刺激扩增ＣＭＬ患者骨髓和外周血单个核细胞（ＭＮＣ）。结果：ＣＭＬ缓解期和慢性期均存在对自体和异体ＣＭＬ细胞杀伤活性的Ｔ淋巴细胞，这些细胞对自体和异体正常ＭＮＣ没有杀伤活性，对正常ＣＦＵ－ＧＭ无抑制作用。而ＬＡＫ细胞对自体ＣＭＬ细胞无杀伤活性（＜１０％），只对异体ＣＭＬ细胞有杀伤活性。上述Ｔ细胞包括ＣＤ３＋ＣＤ５６＋非主要组织相容性抗原（ＭＨＣ）限制性Ｔ细胞，和ＣＤ３＋ＣＤ６－ＭＨＣ限制性Ｔ细胞。用自体ＣＭＬ细胞刺激可增加Ｔ细胞激活抗原ＣＤ２５和ＨＬＡ－ＤＲ的表达。上述Ｔ细胞对自体ＣＭＬ细胞呈较弱的增殖反应，对异体ＣＭＬ细胞几乎无增殖反应，对载有ＢＣＲ－ＡＢＬ肽的自体缓解期ＥＢ病毒转染Ｂ细胞也无增殖反应。结论：ＣＭＬ细胞可能有共同的肿瘤抗原，后者可以被Ｔ细胞识别，但尚无证据表明是ｐ２１０的融合区序列。
OBJECTIVE: To verify the presence of cytotoxic T lymphocyte precursor cells in patients with chronic myeloid leukemia (CML) and to identify their phenotypic and functional characteristics. METHODS: Bone marrow and peripheral blood mononuclear cells (MNCs) from patients with CML were stimulated with autologous neoplastic cells and cytokines using a mixed lymphoma cell culture technique. RESULTS: There were T lymphocytes in CML cell killing activity in both remission and chronic phase of CML. These cells had no killing activity on autologous and allogeneic normal MNCs, and had no inhibitory effect on normal CFU-GM. However, LAK cells have no killing activity (<10%) on autologous CML cells, and have killing activity only on allogeneic CML cells. Such T cells include CD3+CD56+ non-major histocompatibility antigen (MHC)-restricted T cells, and CD3+CD6-MHC-restricted T cells. Stimulation with autologous CML cells increases the expression of T cell activating antigens CD25 and HLA-DR. The above T cells showed a weak proliferative response to autologous CML cells, almost no proliferative response to allogeneic CML cells, and no proliferative response to B cells transfected with Epstein-Barr virus in autoremission stage containing the BCR-ABL peptide. CONCLUSIONS: CML cells may have common tumor antigens that can be recognized by T cells, but there is no evidence that the p210 fusion region sequence.