Department of Hematology, Oncology and Tumorimmunology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Front Immunol. 2023 Jan 24;13:1079921. doi: 10.3389/fimmu.2022.1079921. eCollection 2022.
Despite considerable progress in allogeneic hematopoietic cell transplantation (allo-HCT) has been achieved over the past years, chronic Graft-versus-Host Disease (cGvHD) still contributes to high morbidity rates, thus remaining a major hurdle in allo-HCT patients. To understand the complex pathophysiology of cGvHD and to develop refined prophylaxis and treatment strategies, improved pre-clinical models are needed. In this study, we developed two murine cGvHD models, which display high long-term morbidity but low mortality and depict the heterogeneous clinical manifestations of cGvHD seen in patients. We established a haploidentical C57BL/6→B6D2F1 allo-HCT model that uses myeloablative radiation and G-CSF-mobilized splenocytes as stem cell source and a sub-lethally irradiated Xenograft model, which utilizes the transfer of human peripheral blood mononuclear cells (PBMCs) into NOD scid gamma (NSG)-recipients. We characterized both mouse models to exhibit diverse clinical and histopathological signs of human cGvHD as extensive tissue damage, fibrosis/sclerosis, inflammation and B cell infiltration in cGvHD target organs skin, liver, lung and colon and found a decelerated immune cell reconstitution in the late phase after HCT. Our pre-clinical models can help to gain a deeper understanding of the target structures and mechanisms of cGvHD pathology and may enable a more reliable translation of experimental findings into the human setting of allo-HCT.
尽管过去几年异基因造血细胞移植(allo-HCT)取得了相当大的进展,但慢性移植物抗宿主病(cGvHD)仍然导致高发病率,因此仍然是 allo-HCT 患者的主要障碍。为了了解 cGvHD 的复杂病理生理学,并制定更精细的预防和治疗策略,需要改进临床前模型。在这项研究中,我们开发了两种小鼠 cGvHD 模型,它们具有高长期发病率但低死亡率,并描绘了患者中所见的 cGvHD 的异质临床表现。我们建立了一种半同基因 C57BL/6→B6D2F1 allo-HCT 模型,该模型使用骨髓清除性辐射和 G-CSF 动员的脾细胞作为干细胞来源,以及一种亚致死性照射的异种移植物模型,该模型利用人外周血单核细胞(PBMC)转移到 NOD scid gamma(NSG)-受体中。我们对这两种小鼠模型进行了表征,都表现出广泛的组织损伤、纤维化/硬化、炎症和 B 细胞浸润等人类 cGvHD 的多种临床和组织病理学特征,在 HCT 后晚期观察到免疫细胞重建的减速。我们的临床前模型可以帮助更深入地了解 cGvHD 病理学的靶结构和机制,并可能更可靠地将实验结果转化为 allo-HCT 的人类环境。