Division of Laboratory and Genomic Medicine, Department of Pathology and Immunology and.
Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
J Clin Invest. 2021 Dec 15;131(24). doi: 10.1172/JCI145501.
Despite the curative potential of hematopoietic stem cell transplantation (HSCT), conditioning-associated toxicities preclude broader clinical application. Antibody-drug conjugates (ADCs) provide an attractive approach to HSCT conditioning that minimizes toxicity while retaining efficacy. Initial studies of ADC conditioning have largely focused on syngeneic HSCT. However, to treat acute leukemias or induce tolerance for solid organ transplantation, this approach must be expanded to allogeneic HSCT (allo-HSCT). Using murine allo-HSCT models, we show that pharmacologic Janus kinase 1/2 (JAK1/2) inhibition combined with CD45- or cKit-targeted ADCs enables robust multilineage alloengraftment. Strikingly, myeloid lineage donor chimerism exceeding 99% was achievable in fully MHC-mismatched HSCT using this approach. Mechanistic studies using the JAK1/2 inhibitor baricitinib revealed marked impairment of T and NK cell survival, proliferation, and effector function. NK cells were exquisitely sensitive to JAK1/2 inhibition due to interference with IL-15 signaling. Unlike irradiated mice, ADC-conditioned mice did not develop pathogenic graft-versus-host alloreactivity when challenged with mismatched T cells. Finally, the combination of ADCs and baricitinib balanced graft-versus-host disease and graft-versus-leukemia responses in delayed donor lymphocyte infusion models. Our allo-HSCT conditioning strategy exemplifies the promise of immunotherapy to improve the safety of HSCT for treating hematologic diseases.
尽管造血干细胞移植 (HSCT) 具有治疗潜力,但与预处理相关的毒性限制了其更广泛的临床应用。抗体药物偶联物 (ADC) 为 HSCT 预处理提供了一种有吸引力的方法,可以最大限度地降低毒性,同时保持疗效。ADC 预处理的初始研究主要集中在同基因 HSCT 上。然而,为了治疗急性白血病或诱导实体器官移植耐受,必须将这种方法扩展到异基因 HSCT (allo-HSCT)。使用小鼠 allo-HSCT 模型,我们表明,药物性 Janus 激酶 1/2 (JAK1/2) 抑制与靶向 CD45 或 cKit 的 ADC 联合使用可实现强大的多谱系同种异体植入。引人注目的是,使用这种方法在完全 MHC 错配的 HSCT 中可以实现超过 99%的髓系供体嵌合。使用 JAK1/2 抑制剂巴利昔替尼进行的机制研究表明,T 和 NK 细胞的存活、增殖和效应功能受到明显损害。由于干扰了白细胞介素 15 信号,NK 细胞对 JAK1/2 抑制极为敏感。与辐照小鼠不同,在用错配 T 细胞挑战时,ADC 处理的小鼠不会产生致病性移植物抗宿主同种异体反应。最后,ADC 和巴利昔替尼的组合在延迟供体淋巴细胞输注模型中平衡了移植物抗宿主病和移植物抗白血病反应。我们的 allo-HSCT 预处理策略证明了免疫疗法在提高 HSCT 治疗血液疾病安全性方面的潜力。