Department of Radiation Oncology, Duke University Medical Center, Durham, North Carolina 27710.
Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710.
Radiat Res. 2021 Mar 1;195(3):301-306. doi: 10.1667/RADE-20-00221.1.
Mouse models of radiation-induced thymic lymphoma are commonly used to study the biological effects of total-body irradiation (TBI) on the formation of hematologic malignancies. It is well documented that radiation-induced thymic lymphoma can be inhibited by protecting the bone marrow (BM) from irradiation; however, the mechanisms underlying this phenomenon are poorly understood. Here, we aimed to address this question by performing transplantation of BM cells from genetically engineered mice that have defects in tumor immunosurveillance or occupying different thymic niches. We found that BM cells from mice that have impaired tumor immunosurveillance, by deleting tumor necrosis factor alpha (TNFα), interferon gamma (IFNγ) or perforin-1 (PRF1), remained sufficient to suppress the formation of radiation-induced thymic lymphoma. On the other hand, BM cells from Rag2-/-; γc-/- mice and Rag2-/- mice, which have defects in occupying thymic niches beyond double negative (DN2) and DN3, respectively, failed to inhibit radiation-induced lymphomagenesis in the thymus. Taken together, based on our findings, we propose a model where unirradiated BM cells suppress radiation-induced lymphomagenesis in the thymus by competing with tumor-initiating cells for thymic niches beyond the DN3 stage.
辐射诱导的胸腺淋巴瘤小鼠模型常用于研究全身照射(TBI)对血液恶性肿瘤形成的生物学影响。有充分的文献记载表明,通过保护骨髓(BM)免受辐射照射,可以抑制辐射诱导的胸腺淋巴瘤;然而,这种现象的机制尚不清楚。在这里,我们通过对具有肿瘤免疫监视缺陷或占据不同胸腺龛位的基因工程小鼠的 BM 细胞进行移植,旨在解决这个问题。我们发现,通过删除肿瘤坏死因子-α(TNFα)、干扰素-γ(IFNγ)或穿孔素-1(PRF1),具有肿瘤免疫监视缺陷的小鼠的 BM 细胞仍然足以抑制辐射诱导的胸腺淋巴瘤的形成。另一方面,来自 Rag2-/-;γc-/- 小鼠和 Rag2-/- 小鼠的 BM 细胞,分别在双阴性(DN2)和 DN3 以外的胸腺龛位存在缺陷,无法抑制胸腺中辐射诱导的淋巴瘤发生。综上所述,根据我们的发现,我们提出了一个模型,即未受照射的 BM 细胞通过与肿瘤起始细胞竞争 DN3 阶段以外的胸腺龛位,抑制胸腺中辐射诱导的淋巴瘤发生。