A series of immune abnormalities presenting in aplastic anemia (AA) support the immune pathogenesis of AA. However, how abnormal immunity specifically damages hematopoietic stem cells (HSCs) remains ambiguous. The discovery of bone marrow immune privilege (IP) sites which are composed of CD4 ⁺CD25 ⁺FoxP3 ⁺ regulatory T cells (Tregs) exclusively to protect HSCs prompted us boldly assumed that it is a loss of IP protection leading to HSCs exhausted in AA. A experiment study to clinically confirm the correlation between HSCs depletion and IP abnormalities in patients with AA was conducted. The distribution of Tregs in bone marrow from children with AA, myelodysplastic syndrome (MDS) and control group was detected by immunohistochemistry. Th1, Th2, Th17 and HSCs as well as cytokines in bone marrow of these children were examined by flow cytometry. Tregs near endostea surface of bone marrow of children with AA was significantly lower than that in control and MDS. Th1 was more predominant in AA than in the control children. TNF-α, IFN-γ and IL-17 levels were also increased in AA. Compared to the control group, HSCs in bone marrow of AA, including Long-term HSCs (LT-HSCs) and Short-term HSCs (ST-HSCs), were at lower level. The results indicate that HSCs depletion is closely related to bone marrow IP abnormalities in AA, and the role of IP abnormalities in the pathogenesis of aplastic anemia deserves further research.