The role of interferon (IFN)-γ on thymocyte apoptosis in response to lipopolysaccharide (LPS) was investigated. The administration of LPS into mice induced marked apoptosis of thymocytes in vivo, but the simultaneous injection of anti-IFN-γ antibody with LPS completely prevented thymocyte apoptosis. Pretreatment of mice with IFN-γ markedly enhanced LPS-induced thymocyte apoptosis. Thymocyte apoptosis augmented by IFN-γ occurred in the thymic cortex, and target cells undergoing apoptosis were CD4+8+ immature thymocytes. IFN-γ itself did not induce thymocyte apoptosis in vivo and in vitro. IFN-γ exhibited no synergistic action with effector molecules, such as tumor necrosis factor (TNF)-α and glucocorticoids. Further, it was shown that IFN-γ did not enhance the susceptibility of thymocytes to apoptosis. Pretreatment of mice with IFN-γ significantly augmented the serum TNF-α level and the serum cortisol level in response to LPS. Therefore, we suggest that IFN-γ might augment LPS-induced thymocyte apoptosis through elevating serum TNF-α and cortisol levels.
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