Ling X, Wang Y, Dietrich M F, Andreeff M, Arlinghaus R B
Department of Bone Marrow Transplantation, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Oncogene. 2006 Jul 27;25(32):4483-90. doi: 10.1038/sj.onc.1209477. Epub 2006 Mar 20.
The fundamental basis for immunotherapy of leukemia is that leukemic cells express specific antigens that are not expressed by normal hematopoietic cells. However, the host immune system appears to be tolerant to leukemia cells. To overcome this tolerance, we vaccinated immunocompetent mice with murine leukemia cells (WEHI-3B and BCR-ABL+ 32D cells) transduced with a specifically constructed transmembrane form of granulocyte-macrophage colony-stimulating factor (tmGM-CSF). The transduced cells expressed tmGM-CSF on the cell-surface. To determine whether tmGM-CSF-expressing WEHI-3B leukemia cells would prevent leukemia formation as a vaccine, immunocompetent mice (BALB/c and C3H/HEJ) were immunized with lethally irradiated murine leukemia cells expressing cell-surface tmGM-CSF before challenging mice with murine leukemia cells. Two immunocompetent mouse models were investigated, either WEHI-3B cells in BALB/c mice or BCR-ABL+ 32D cells in C3H/HEJ mouse. The results showed that 100% of WEHI-3B/tmGM-CSF-vaccinated BALB/c mice and about 65% of 32D+ BCR-ABL/tmGM-CSF-vaccinated C3H/HEJ mice were protected from leukemia after leukemia cell challenge, whereas all non-vaccinated mice succumbed to leukemia. Spleen and marrow cell suspensions from vaccinated mice challenged with WEHI-3B cells lacked detectable GFP+ WEHI-3B cells at 82 days post-challenge. A significant delay of death was observed in C3H/HEJ mice challenged with the very aggressive DA-1 cell line expressing BCR-ABL. Vaccination of mice with WEHI-3B/CD40L cells protected 80% of the mice from the WEHI-3B challenge. Notably, 60% of the WEHI-3B/BALB/c mice were also protected from leukemia when WEHI-3B/tmGM-CSF vaccination was carried out after the leukemia challenge. In order to determine whether cellular immunity is involved in this vaccine-mediated protection, either CD4+ or CD8+ T cells were depleted from mice after the WEHI-3B/tmGM-CSF vaccination. The results indicate that CD8+ T-cells mediated the protective immune response provided by the irradiated tmGM-CSF-expressing WEHI-3B cells. In addition, vaccination of nude mice did not provide protection from WEHI-3B leukemia induction. Importantly, 80% of non-vaccinated mice were also protected from a WEHI-3B cell challenge after receiving spleen cells from vaccinated mice 1 day before challenge with leukemia cells. These results indicate that overexpression of tmGM-CSF on the leukemia cell-surface can enhance the recognition of leukemic cells by CD8+ T cells, and can either prevent or significantly delay leukemia induction. These findings suggest that injection of irradiated leukemia cells expressing cell-surface-bound GM-CSF has the potential as an immunological approach to treat leukemia.
白血病免疫疗法的基本依据是白血病细胞表达正常造血细胞所不表达的特异性抗原。然而,宿主免疫系统似乎对白血病细胞具有耐受性。为了克服这种耐受性,我们用经特异性构建的跨膜形式的粒细胞 - 巨噬细胞集落刺激因子(tmGM - CSF)转导的鼠白血病细胞(WEHI - 3B和BCR - ABL + 32D细胞)对免疫活性小鼠进行疫苗接种。转导后的细胞在细胞表面表达tmGM - CSF。为了确定表达tmGM - CSF的WEHI - 3B白血病细胞作为疫苗是否能预防白血病形成,在用鼠白血病细胞攻击小鼠之前,用经致死性照射的、表达细胞表面tmGM - CSF的鼠白血病细胞对免疫活性小鼠(BALB / c和C3H / HEJ)进行免疫接种。研究了两种免疫活性小鼠模型,即BALB / c小鼠中的WEHI - 3B细胞或C3H / HEJ小鼠中的BCR - ABL + 32D细胞。结果显示,接种WEHI - 3B / tmGM - CSF的BALB / c小鼠中有100%以及接种32D + BCR - ABL / tmGM - CSF的C3H / HEJ小鼠中有约65%在白血病细胞攻击后免受白血病侵害,而所有未接种疫苗的小鼠均死于白血病。在用WEHI - 3B细胞攻击的接种疫苗小鼠的脾脏和骨髓细胞悬液中,在攻击后82天未检测到绿色荧光蛋白(GFP)阳性的WEHI - 3B细胞。在用表达BCR - ABL的极具侵袭性的DA - 1细胞系攻击的C3H / HEJ小鼠中观察到死亡明显延迟。用WEHI - 3B / CD40L细胞对小鼠进行疫苗接种可使80%的小鼠免受WEHI - 3B攻击。值得注意的是,当在白血病攻击后进行WEHI - 3B / tmGM - CSF疫苗接种时,60%的WEHI - 3B / BALB / c小鼠也免受白血病侵害。为了确定细胞免疫是否参与这种疫苗介导的保护作用,在WEHI - 3B / tmGM - CSF疫苗接种后从小鼠体内清除CD4 +或CD8 + T细胞。结果表明,CD8 + T细胞介导了经照射的表达tmGM - CSF的WEHI - 3B细胞提供的保护性免疫反应。此外,对裸鼠进行疫苗接种不能预防WEHI - 3B白血病的诱导。重要的是,80%未接种疫苗的小鼠在白血病细胞攻击前1天接受接种疫苗小鼠的脾细胞后,也免受WEHI - 3B细胞攻击。这些结果表明,白血病细胞表面tmGM - CSF的过表达可增强CD8 + T细胞对白血病细胞的识别,并可预防或显著延迟白血病的诱导。这些发现表明,注射表达细胞表面结合型GM - CSF的经照射白血病细胞具有作为治疗白血病的免疫方法的潜力。