| Autor: |
Huang G; Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China., Zhang Y; Department of Hematology, Guangzhou First People's Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China., Wei X; Department of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, China., Yu Z; Department of Hematology, First Affiliated Hospital, Jinan University, Guangzhou, China., Lai J; Department of Hematology, First Affiliated Hospital, Jinan University, Guangzhou, China., Shen Q; Department of Hematology, Second Clinical Medical College of Jinan University (Shenzhen People's Hospital), Shengzhen, China., Chen X; Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China., Tan G; Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China., Chen C; Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China., Luo W; Guangzhou Blood Center, Guangzhou, China., Li Y; Department of Hematology, Guangzhou First People's Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China., Zhou M; Department of Hematology, Guangzhou First People's Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China., Li Y; Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China., Li B; Institute of Hematology, School of Medicine, Jinan University, Guangzhou, China. |
| Abstrakt: |
Aplastic anemia (AA) is a T cell immune-mediated autoimmune disease. Overactivated CD8 + T cells play a leading role in the pathogenesis of AA, which may be due to disbalance in costimulatory and coinhibitory signals in T cells. In this study, we firstly investigated the expression of OX40, 4-1BB, GITR, ICOS, CTLA-4, LAG-3, and TIM-3 on CD8 + T cells from untreated patients with AA and healthy individuals (HIs) by flow cytometry. Moreover, we further analyzed the phenotype and functional characteristics of CD8 + GITR + T cells to more fully assess the T cell activation dysfunction in AA. We for the first time demonstrated significantly decreased percentage of CD8 + GITR + T cells in AA, and CD8 + GITR + CTLA-4 + T cells were significantly higher in patients with AA compared with HIs. Conversely, the percentage of CD8 + GITR + granzyme B + and CD8 + GITR + perforin + T cells in AA patients was significantly reduced. Our preliminary data illustrate that the CD8 + GITR + T cell population might negatively regulate overactive T cell activation in AA. |
