Miyake Takashi, Hosaka Naoki, Cui Wenhao, Nishida Teruhisa, Takaki Takashi, Inaba Muneo, Kamiyama Yasuo, Ikehara Susumu
First Department of Pathology, Kansai Medical University, Moriguchi, Osaka, Japan.
Immunology. 2009 Apr;126(4):552-64. doi: 10.1111/j.1365-2567.2008.02920.x. Epub 2008 Sep 4.
Although allogeneic bone marrow transplantation (BMT) plus donor lymphocyte infusion (DLI) is performed for solid tumours to enhance graft-versus-tumour (GVT) effects, a graft-versus-host reaction (GVHR) is also elicited. We carried out intra-bone marrow-bone marrow transplantation (IBM-BMT) plus adult thymus transplantation (ATT) from the same donor to supply alloreactive T cells continually. Normal mice treated with IBM-BMT + ATT survived for a long time with high donor-derived thymopoiesis and mild GVHR. The percentage of CD4(+) FoxP3(+) regulatory T cells in the spleen of the mice treated with IBM-BMT + ATT was lower than in normal B6 mice or mice treated with IBM-BMT alone, but higher than in mice treated with IBM-BMT + DLI; the mice treated with IBM-BMT + DLI showed severe GVHR. In tumour-bearing mice, tumour growth was more strongly inhibited by IBM-BMT + ATT than by IBM-BMT alone. Mice treated with IBM-BMT + a high dose of DLI also showed tumour regression comparable to that of mice treated with IBM-BMT + ATT but died early of GVHD. By contrast, mice treated with IBM-BMT + a low dose of DLI showed longer survival but less tumour regression than the mice treated with IBM-BMT + ATT. Histologically, significant numbers of CD8(+) T cells were found to have infiltrated the tumour in the mice treated with IBM-BMT + ATT. The number of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labelling (TUNEL)-positive apoptotic tumour cells also significantly increased in the mice treated with IBM-BMT + ATT. Allogeneic IBM-BMT + ATT thus can induce high thymopoiesis, preserving strong GVT effects without severe GVHR.
尽管进行异基因骨髓移植(BMT)加供体淋巴细胞输注(DLI)用于实体瘤以增强移植物抗肿瘤(GVT)效应,但也会引发移植物抗宿主反应(GVHR)。我们进行了同基因供体的骨髓内骨髓移植(IBM-BMT)加成年胸腺移植(ATT),以持续提供同种反应性T细胞。接受IBM-BMT + ATT治疗的正常小鼠存活时间长,具有高水平的供体来源胸腺生成和轻度GVHR。接受IBM-BMT + ATT治疗的小鼠脾脏中CD4(+) FoxP3(+)调节性T细胞的百分比低于正常B6小鼠或仅接受IBM-BMT治疗的小鼠,但高于接受IBM-BMT + DLI治疗的小鼠;接受IBM-BMT + DLI治疗的小鼠表现出严重的GVHR。在荷瘤小鼠中,IBM-BMT + ATT比单独的IBM-BMT更强烈地抑制肿瘤生长。接受IBM-BMT +高剂量DLI治疗的小鼠也表现出与接受IBM-BMT + ATT治疗的小鼠相当的肿瘤消退,但因移植物抗宿主病(GVHD)过早死亡。相比之下,接受IBM-BMT +低剂量DLI治疗的小鼠存活时间更长,但肿瘤消退比接受IBM-BMT + ATT治疗的小鼠少。组织学上,在接受IBM-BMT + ATT治疗的小鼠中发现大量CD8(+) T细胞浸润肿瘤。接受IBM-BMT + ATT治疗的小鼠中,末端脱氧核苷酸转移酶介导的dUTP生物素缺口末端标记(TUNEL)阳性凋亡肿瘤细胞的数量也显著增加。因此,异基因IBM-BMT + ATT可诱导高水平的胸腺生成,在不引发严重GVHR的情况下保留强大的GVT效应。