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.
Keywords: Aplastic anemia; T cell activation; glucocorticoid-induced tumor necrosis factor receptor.