Aplastic anemia, an uncommon and life-threatening blood disorder, is featured by pancytopenia and trilineage bone marrow (BM) aplasia. 1 Aplastic anemia is considered as a special autoimmune disease that targeting the BM. Aberrant immunity, mainly autoreactive T lymphocytes attacking on hemopoietic progenitor cells, has been considered to play indispensably crucial roles in the pathogenesis of aplastic anemia. [1][2][3][4] Abnormally polarized Th1 cells, elevated Th17 cells, and activated CD8 + cytotoxic T cells were proven to be involved in the immune-mediated damage of hematopoiesis by the following two ways: indirect induction of hematopoietic cells apoptosis by excessively releasing hematopoietic negative regulators, such as interferon (IFN)γ and tumor necrosis factor (TNF)α; and direct damage to autologous hematopoietic stem cells. [4][5][6][7] Further analysis confirmed that regulatory T cells (Tregs) and other cytokines, for