Dangi Anil, Yu Shuangjin, Lee Frances T, Burnette Melanie, Wang Jiao-Jing, Kanwar Yashpal S, Zhang Zheng J, Abecassis Michael, Thorp Edward B, Luo Xunrong
Nephrology, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA.
Nephrology, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA; Division of Organ Transplantation, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Kidney Int. 2020 Jul;98(1):147-158. doi: 10.1016/j.kint.2020.01.034. Epub 2020 Feb 21.
Cytomegalovirus (CMV) reactivation from latently infected donor organs post-transplantation and its dissemination cause significant comorbidities in transplant recipients. Transplant-induced inflammation combined with chronic immunosuppression has been thought to provoke CMV reactivation and dissemination, although sequential events in this process have not been studied. Here, we investigated this process in a high-risk donor CMV-positive to recipient CMV-negative allogeneic murine kidney transplantation model. Recipients were either treated with indefinite immunosuppression or tolerized in a donor-specific manner. Untreated recipients served as controls. Kidney allografts from both immunosuppressed and tolerized recipients showed minimal alloimmunity-mediated graft inflammation and normal function for up to day 60 post-transplantation. However, despite the absence of such inflammation in the immunosuppressed and tolerized groups, CMV reactivation in the donor positive kidney allograft was readily observed. Interestingly, subsequent CMV replication and dissemination to distant organs only occurred in immunosuppressed recipients in which CMV-specific CD8 T cells were functionally impaired; whereas in tolerized recipients, host anti-viral immunity was well-preserved and CMV dissemination was effectively prevented. Thus, our studies uncoupled CMV reactivation from its dissemination, and underscore the potential role of robust transplantation tolerance in preventing CMV diseases following allogeneic kidney transplantation.
移植后潜伏感染的供体器官中巨细胞病毒(CMV)再激活及其传播会在移植受者中引发严重的合并症。移植诱导的炎症与慢性免疫抑制相结合被认为会引发CMV再激活和传播,尽管这一过程中的一系列事件尚未得到研究。在此,我们在高危供体CMV阳性至受体CMV阴性的同种异体小鼠肾移植模型中研究了这一过程。受体要么接受无限期免疫抑制治疗,要么以供体特异性方式实现免疫耐受。未治疗的受体作为对照。免疫抑制和免疫耐受受体的肾移植在移植后60天内均表现出最小的同种免疫介导的移植炎症和正常功能。然而,尽管免疫抑制和免疫耐受组没有这种炎症,但在供体阳性的肾移植中很容易观察到CMV再激活。有趣的是,随后的CMV复制和向远处器官的传播仅发生在CMV特异性CD8 T细胞功能受损的免疫抑制受体中;而在免疫耐受受体中,宿主抗病毒免疫得到良好保存,CMV传播得到有效预防。因此,我们的研究将CMV再激活与其传播分离开来,并强调了强大的移植耐受性在预防同种异体肾移植后CMV疾病中的潜在作用。