Brucella abortus induces a novel cytokine gene expression pattern characterized by elevated IL-10 and IFN-gamma in CD4+ T cells

• Published in: International immunology Vol. 5; no. 8; p. 877
• Main Authors: Svetić, A, Jian, Y C, Lu, P, Finkelman, F D, Gause, W C
• Format: Journal Article
• Language: English
• Published: England 01-08-1993
• Subjects: Animals; Brucella abortus - immunology; CD4-Positive T-Lymphocytes - metabolism; Female; Gene Expression Regulation; Immunization; Interferon-gamma - biosynthesis; Interferon-gamma - genetics; Interleukin-10 - biosynthesis; Interleukin-10 - genetics; Interleukin-2 - physiology; Mice; Mice, Inbred BALB C; T-Lymphocytes, Helper-Inducer - metabolism
• ISSN: 0953-8178
• DOI: 10.1093/intimm/5.8.877

Immunization of BALB/c mice with killed Brucella abortus (BA) has previously been shown to increase serum IgG2a levels and long-term T cell clones from these mice secrete Th1-associated cytokines: IFN-gamma and IL-2 but not IL-4 or IL-5. We analyzed cytokine gene expression following primary immunization with BA to determine when CD4+ T cells first express cytokine genes and whether specific hypothesized cytokine patterns (e.g. Th precursor, Th0) could be identified prior to a Th1-like pattern. Our results demonstrated a highly consistent and novel pattern of Th1/Th2 cytokine gene expression characterized by elevated IL-10 and IFN-gamma in CD4+ T cells which rapidly manifests itself and is sustained for at least 10 days after immunization. No elevation in IL-2 cytokine gene expression was observed and treatment of BA-immunized mice with blocking anti-IL-2 antibodies had no effect on the cytokine gene expression pattern, although treatment with anti-IFN antibodies resulted in increased IL-4, IL-5, and IL-9 cytokine gene expression, in the absence of any change in IFN-gamma or IL-10 as early as 4 days after immunization. These results suggest that a whole pathogen may trigger sufficient costimulatory signals to rapidly induce effector T cells in the absence of elevated IL-2 and that IL-10 is specifically elevated in certain Th1-like responses.