Augmentation of Lipopolysaccharide-Induced Thymocyte Apoptosis by Interferon-γ

• Published in: Cellular immunology 1997-05, Vol.177 (2), p.103-108
• Main Authors: Kato, Yutaka, Morikawa, Akiko, Sugiyama, Tsuyoshi, Koide, Naoki, Jiang, Guo-Zhi, Lwin, Tin, Yoshida, Tomoaki, Yokochi, Takashi
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis - drug effects; Drug Synergism; Hydrocortisone - blood; Hydrocortisone - pharmacology; Interferon-gamma - pharmacology; Lipopolysaccharides - pharmacology; Mice; Mice, Inbred BALB C; Recombinant Proteins; T-Lymphocytes - cytology; T-Lymphocytes - drug effects; Thymus Gland - cytology; Thymus Gland - drug effects; Tumor Necrosis Factor-alpha - analysis; Tumor Necrosis Factor-alpha - pharmacology
• ISSN: 0008-8749; 1090-2163
• DOI: 10.1006/cimm.1997.1103

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 thymocytesin 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 apoptosisin vivoandin 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.