Human CMV infection is frequent in kidney transplant recipients (KTR). Pretransplant Ag-specific T cells and adaptive NKG2C⁺ NK cells associate with reduced incidence of infection in CMV⁺ KTR. Expansions of adaptive NKG2C⁺ NK cells were reported in posttransplant CMV-infected KTR. To further explore this issue, NKG2C⁺ NK, CD8⁺, and TcRγδ T cells were analyzed pretransplant and at different time points posttransplant for ≥24 mo in a cohort of CMV⁺ KTR (n = 112), stratified according to CMV viremia detection. In cryopreserved samples from a subgroup (n = 49), adaptive NKG2C⁺ NK cell markers and T cell subsets were compared after a longer follow-up (median, 56 mo), assessing the frequencies of CMV-specific T cells and viremia at the last time point. Increased proportions of NKG2C⁺ NK, CD8⁺, and TcRγδ T cells were detected along posttransplant evolution in viremia(+) KTR. However, the individual magnitude and kinetics of the NKG2C⁺ NK response was variable and only exceptionally detected among viremia(–) KTR, presumably reflecting subclinical viral replication events. NKG2C⁺ expansions were independent of KLRC2 zygosity and associated with higher viral loads at diagnosis; no relation with other clinical parameters was perceived. Increased proportions of adaptive NKG2C⁺ NK cells (CD57⁺, ILT2⁺, FcεRIγ^–) were observed after resolution of viremia long-term posttransplant, coinciding with increased CD8⁺ and Vδ2^– γδ T cells; at that stage CMV-specific T cells were comparable to viremia(–) cases. These data suggest that adaptive NKG2C⁺ NK cells participate with T cells to restore CMV replication control, although their relative contribution cannot be discerned.

人 CMV 感染在肾移植受者 (KTR) 中很常见。移植前 Ag 特异性 T 细胞和适应性 NKG2C ⁺ NK 细胞与 CMV ⁺ KTR中感染的发生率降低有关。在移植后 CMV 感染的 KTR 中报道了适应性 NKG2C ⁺ NK 细胞的扩增。为了进一步探讨这个问题，在 CMV ⁺ KTR队列（n = 112）中，根据 CMV 病毒血症检测分层，在移植前和移植后不同时间点对NKG2C ⁺ NK、CD8 ⁺和 TcRγδ T 细胞进行了分析，≥24 个月。在来自亚组 ( n = 49) 的冷冻保存样本中，自适应 NKG2C ⁺在较长的随访时间（中位数，56 个月）后比较了 NK 细胞标志物和 T 细胞亚群，评估了最后一个时间点 CMV 特异性 T 细胞和病毒血症的频率。在病毒血症 (+) KTR 中，随着移植后进化，检测到NKG2C ⁺ NK、CD8 ⁺和 TcRγδ T 细胞的比例增加。然而，NKG2C ⁺ NK 反应的个体幅度和动力学是可变的，并且仅在病毒血症（-）KTR 中异常检测到，大概反映了亚临床病毒复制事件。NKG2C ⁺扩增与KLRC2 合子性无关，并与诊断时较高的病毒载量有关；与其他临床参数没有关系。增加自适应 NKG2C 的比例⁺ NK 细胞（CD57 ⁺、ILT2 ⁺、FcεRIγ ^–）在长期移植后病毒血症消退后观察到，同时增加了 CD8 ⁺和 Vδ2 ^– γδ T 细胞；在那个阶段，CMV 特异性 T 细胞与病毒血症（-）病例相当。这些数据表明适应性 NKG2C ⁺ NK 细胞与 T 细胞一起恢复 CMV 复制控制，尽管无法辨别它们的相对贡献。