Abstract
IL-18 (interferon-inducing factor) and IL-12 exhibit a marked synergism in interferon-gamma induction in T cells. Investigations into the mechanism of this synergism have revealed that IL-12 upregulates expression of the IL-18 receptor on cells producing interferon-gamma. Although IL-18 does not induce the development of Th1 cells, it is essential for the effective induction and activation of Th1 cells by IL-12. As for natural killer cells, IL-18 seems to activate them independently of IL-12. Although IL-12 and IL-18 activate both innate and acquired immunity, their excessive production by activated macrophages may induce multiple organ disorders including disruption of the immune system.
MeSH terms
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Animals
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B-Lymphocytes / drug effects
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B-Lymphocytes / metabolism
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Cells, Cultured
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Cytokines / pharmacology*
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Cytokines / physiology
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Cytokines / toxicity
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Drug Synergism
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Gene Expression Regulation / drug effects*
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Immunoglobulin E / biosynthesis
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Interferon-gamma / biosynthesis*
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Interferon-gamma / genetics
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Interleukin-12 / pharmacology*
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Interleukin-12 / physiology
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Interleukin-12 / toxicity
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Interleukin-18
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Interleukin-18 Receptor alpha Subunit
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Killer Cells, Natural / drug effects*
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Killer Cells, Natural / metabolism
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Macrophage Activation
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Macrophages / immunology
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Macrophages / metabolism
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Mice
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Mice, Inbred BALB C
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Models, Immunological
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RNA, Messenger / biosynthesis
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Receptors, Interleukin / biosynthesis
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Receptors, Interleukin / genetics
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Receptors, Interleukin-18
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Signal Transduction
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T-Lymphocytes / drug effects*
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T-Lymphocytes / metabolism
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Th1 Cells / drug effects
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Th1 Cells / immunology
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Up-Regulation / drug effects
Substances
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Cytokines
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Il18r1 protein, mouse
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Interleukin-18
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Interleukin-18 Receptor alpha Subunit
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RNA, Messenger
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Receptors, Interleukin
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Receptors, Interleukin-18
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Interleukin-12
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Immunoglobulin E
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Interferon-gamma