热休克体外诱导自身T细胞对慢性髓系白血病细胞的杀伤

目的 研究热休克对慢性髓系白血病（ＣＭＬ）患自身Ｔ细胞杀伤（ＡＴＫ）肿瘤细胞活性的影响。方法 用＾５１Ｃｒ释放法检测自身Ｔ细胞对热休克处理的ＣＭＬ靶细胞（△ＣＭＬ）和未灯克处理的ＣＭＬ靶细胞（δＣＭＬ）的ＡＴＫ活性，用流式细胞仪检测ＣＭＬ细胞热休克蛋白７０（ＨＳＰ７０）的表达，淋巴细胞混合培养（ＭＬＴＣ）法刺激扩增Ｔ细胞，并检测其免疫表才ＡＴＫ活性。结果 ２１例ＣＭＬ患中有４例显示对δＣＭＬ有

In vitro induction of autologous T cell killing by heat treated human chronic myelogenous leukemia cells

OBJECTIVE: To investigate the potential of autologous T cell killing of heat treated chronic myelogenous leukemia (CML) cells (autologous tumor killing, ATK). METHODS: (51)Cr release assay was used to measure the ATK activity of autologous T cells against CML cells treated with 42 degrees C for 30 minutes (heat) or 37 degrees C for 30 minutes (non-heat). The phenotypes of T cells and heat shock protein 70 (HSP70) expression of CML cells were measured by flow cytometry (FCM). T cells from the CML patients were stimulated and expanded by autologous mixed lymphocyte/tumor cell cultures (MLTC). RESULTS: ATK activity of autologous T cells to the non-heated and heated CML cells were found in 4 (19.05%) and 10 (47.62%) of the 21 cases, respectively. The ATK activity of interleukin-2 (IL-2) stimulated autologous T cells against heated CML cells was markedly higher than that of unstimulated autologous T cells against non-heated CML cells (P < 0.001). FCM analysis showed that no HSP70 was expressed on the CML cell membranes whether heated or non-heated, but intracellular HSP70 expressions were (83.42 +/- 5.65)% and (78.34 +/- 6.32)% pre- and post-heated, respectively. The phenotypes of T cells stimulated and expanded in MLTC were TCRgammadelta - CD(3)(+), mostly CD(8)(+), with some activation markers (CD(25) and HLA-DR) expression. The ATK activities of these T cells against the heated and non-heated CML cells and K562 cells were (51.25 +/- 4.26)%, (36.52 +/- 3.83)% and (2.92 +/- 1.19)%, respectively. CONCLUSIONS: ATK activity of autologous T cells against CML cells could be induced or enhanced by heat treatment of the CML cells particularly of T cells stimulated with IL-2. This ATK activity was not associated with gammadelta T cells or HSP70 expression of CML cells.