RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
低移植物恒定自然杀伤 T 细胞剂量是同种异体造血细胞移植后巨细胞病毒再激活的危险因素
英文原题：Low Graft Invariant Natural Killer T-Cell Dose Is a Risk Factor for Cytomegalovirus Reactivation After Allogeneic Hematopoietic Cell Transplantation.
查看英文原题
Low Graft Invariant Natural Killer T-Cell Dose Is a Risk Factor for Cytomegalovirus Reactivation After Allogeneic Hematopoietic Cell Transplantation.
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中文摘要
巨细胞病毒（CMV）再激活在同种异体造血细胞移植（HCT）后很常见，并可能导致致命的CMV疾病。恒定自然杀伤T（iNKT）细胞是免疫系统的强效调节因子，可预防移植物抗宿主病，同时促进移植物抗白血病效应。据认为，iNKT细胞选择性影响固有免疫和适应性免疫的介质。在此，我们研究了移植物中iNKT细胞对接受同种异体HCT患者CMV再激活的影响。我们发现，在同种异体移植物中iNKT细胞数量较高的患者中，CMV再激活的累积发生率显著降低。因此，富含iNKT细胞的移植物或过继转移iNKT细胞是改善同种异体HCT后结局的有力细胞治疗策略。
展开英文摘要原文
Cytomegalovirus (CMV) reactivation is common after allogeneic hematopoietic cell transplantation (HCT) and may result in fatal CMV disease. Invariant natural killer T (iNKT) cells are potent modulators of the immune system preventing graft-versus-host disease while promoting graft-versus-leukemia effects. It is thought that iNKT cells selectively influence mediators of both innate and adaptive immunity.
Here, we investigated the impact of graft iNKT cells on CMV reactivation in patients undergoing allogeneic HCT.
We found a significantly decreased cumulative incidence of CMV reactivation in patients with higher numbers of iNKT cells in the allograft.
Therefore iNKT-cell-enriched grafts or adoptive transfer of iNKT cells are compelling cytotherapeutic strategies to improve outcomes after allogeneic HCT.
论文信息
- 作者
- Schneidawind D、Duerr-Stoerzer S、Liewer S、Renner S、Sánchez Navarro B、Atar D、Keppeler H、Beck R
- 单位
- Department of Medicine II, University Hospital Tuebingen, Tuebingen, Germany. Electronic address: dominik.schneidawind@med.uni-tuebingen.de.Germany
- 文献类型
- 非美国政府资助研究
- 期刊
- Transplantation and cellular therapy2022 Aug
- 原文标识
- PubMed 35580734 · DOI 10.1016/j.jtct.2022.05.011