Background: In clinical studies, the findings on sulfur mustard(SM) toxicity for CD3+CD4+ and CD3+CD8+ T lymphocyte subsets are contradictory. In animal experiments, the effect of SM on the T cell number and proliferation is incompatible and is even the opposite of the results in human studies. In this study, we observed the dynamic changes of T lymphocytes in the first week in a high-dose SM-induced model.Methods: Mice were exposed to SM by subcutaneous injection(20 mg/kg) and were sacrificed 4 h, 24 h, 72 h and 168 h later. Spleen T lymphocyte proliferation was evaluated by 3H-Td R. Flow cytometric analysis was used to observe the percentage of CD3+CD4+ and CD3+CD8+ T lymphocyte subsets. The IL-1e assayed using the Luminex method. DNA damage in bone marrow ceβ, IL-6, IL-10 and TNF-lls was observed with α levels in plasma werthe single cell gel electrophoresis technique(SCGE).Results: SM continuously inhibited the proliferation of lymphocytes for 7 days, and there was a significant rebound of Con A-induced T lymphocyte proliferation only at 24 h. The percentage of CD3+CD4+ and CD3+CD8+ lymphocytes was upregulated, which was accompanied by increased IL-1β and TNF-creased in the PG group at 4 h. The peak of lymphocytic apoptα and decreased IL-10. The IL-6 level was gradually deosis and DNA damage occurred at 24 h and 72 h, respectively. Conclusion: Our results show that SM significantly inhibited T lymphocyte proliferation as well as induced CD3+CD4+ and CD3+CD8+ upregulation. SM intoxication also significantly increased the levels of pro-inflammatory cytokines(IL-1β, IL-6 and TNF-α) and inhibited the level of anti-inflammatory cytokine IL-10. Our results may partly be due to the significant SM induced significant apoptosis and necrosis of lymphocytes as well as DNA damage of bone marrow cells. The results provided a favorable evaluation of SM immune toxicity in an animal model. Background: In clinical studies, the findings on sulfur mustard (SM) toxicity for CD3 + CD4 + and CD3 + CD8 + T lymphocyte subsets are contradictory. In animal experiments, the effect of SM on the T cell number and proliferation is incompatible and is even the opposite of the results in human studies. In this study, we observed the dynamic changes of T lymphocytes in the first week in a high-dose SM-induced model. Methods: Mice were exposed to SM by subcutaneous injection (20 mg / kg) and were sacrificed 4 h, 24 h, 72 h and 168 h later. Spleen T lymphocyte proliferation was evaluated by 3H-Td R. Flow cytometric analysis was used to observe the percentage of CD3 + CD4 + and CD3 + CD8 + T lymphocyte subsets. IL-1e assayed using the Luminex method. DNA damage in bone marrow ceβ, IL-6, IL-10 and TNF-lls was observed with α levels in plasma werthe single cell gel electrophoresis technique (SCGE). Results: SM continuously inhibited the proliferation of lymphocytes for 7 days, and there was a significant rebound of Con A-induced T lymphocyte proliferation only at 24 h. The percentage of CD3 + CD4 + and CD3 + CD8 + lymphocytes was upregulated, which was accompanied by increased IL-1β and TNF-creased in the PG group at 4 h. The peak of lymphocytic apoptosis α and decreased IL-10. The IL-6 level was gradually deosis and DNA damage occurred at 24 h and 72 h, respectively. Conclusion: Our results show that SM significantly inhibited T lymphocyte proliferation as induced CD3 + CD4 + and CD3 + CD8 + upregulation. SM intoxication also significantly increased the levels of pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) and inhibited the level of anti-inflammatory cytokine IL-10. the significant SM induced significant apoptosis and necrosis of lymphocytes as well as DNA damage of bone marrow cells. The results provided a favorable evaluation of SM immune toxicity in an animal model.