Immunosuppression characterized by increased Treg cell and IL-10 levels in benzene-induced hematopoietic toxicity mouse model.

Benzene is a typical hematopoietic toxic substance, that can cause serious blood and circulatory system diseases such as aplastic anemia, myelodysplastic syndrome and acute myeloid leukemia, but the immunological mechanism by which this occurs is not clear. T helper cells play a key role in regulating the immune balance in the body. In this study, benzene-induced hematopoietic toxicity BALB/c mice model was established, and changes in immune organs and T helper cell subsets (Th1, Th2, Th17 and Treg cells) were explored. At 28 days after subcutaneous injection of 150 mg/kg benzene, mice showed pancytopenia and obvious pathological damage to the bone marrow, spleen, and thymus. Flow cytometry revealed that the number of CD4+CD25+Foxp3+ Treg cells in the spleen increased significantly. The level of IL-10 in the spleen, serum, and bone marrow increased, while the levels of IL-17 in the spleen and serum decreased. Furthermore, the levels of CD4 and CD8 proteins in the spleen decreased. Immunofluorescence results showed that levels of Foxp3, a specific transcription factor that induced the differentiation of Treg cells, increased after exposure to benzene. Our results demonstrate that immunosuppression occurred in the benzene-induced hematopoietic toxicity model mice, and Treg cells and secreted IL-10 may play a key role in the process.