Podlech J, Holtappels R, Wirtz N, Steffens H P, Reddehase M J
Institute for Virology, Johannes Gutenberg University, Mainz, Germany.
J Gen Virol. 1998 Sep;79 ( Pt 9):2099-104. doi: 10.1099/0022-1317-79-9-2099.
Cytomegalovirus (CMV) infection in the period of temporary immunodeficiency after haematoablative treatment and bone marrow transplantation (BMT) is associated with a risk of graft failure and multiple-organ CMV disease. The efficacy of immune system reconstitution is decisive for the prevention of CMV pathogenesis after BMT. Previous data in murine model systems have documented a redundancy in the immune effector mechanisms controlling CMV. CD8 T cells proved to be relevant but not irreplaceable as antiviral effectors. Specifically, in a state of long-term in vivo depletion of the CD8 T-cell subset, CD4 T cells were educed to become deputy effectors controlling CMV by a mechanism involving antiviral cytokines. It is of medical importance to know whether one can trust in this 'flexible defence' in all clinical settings. It is demonstrated here that reconstitution of CD8 T cells is crucial for the prevention of fatal multiple-organ CMV disease under the specific conditions of BMT.
在清髓性治疗和骨髓移植(BMT)后的暂时免疫缺陷期,巨细胞病毒(CMV)感染与移植物失败和多器官CMV疾病的风险相关。免疫系统重建的效果对于预防BMT后的CMV发病机制至关重要。先前在小鼠模型系统中的数据证明,控制CMV的免疫效应机制存在冗余。CD8 T细胞被证明是相关的,但作为抗病毒效应器并非不可替代。具体而言,在CD8 T细胞亚群长期体内耗竭的状态下,CD4 T细胞通过一种涉及抗病毒细胞因子的机制被诱导成为控制CMV的替代效应器。了解在所有临床环境中是否可以信赖这种“灵活防御”具有医学重要性。此处证明,在BMT的特定条件下,CD8 T细胞的重建对于预防致命的多器官CMV疾病至关重要。