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/ß and IL-18 Synergistically Enhance IFN-
Gene Expression in Human T Cells1
*
Department of Virology, National Public Health Institute, Helsinki, Finland; and
Fujisaki Institute, Hayashibara Biochemical Laboratories, Okayama, Japan
T cells contribute significantly the to host’s early defense
against viral and bacterial infections and are essential for clearance
of the pathogen. IFN-
, a product of activated T and NK cells, has,
in addition to its direct antimicrobial activity, a major role in
activating cell-mediated immunity. Here we report that cytokines
secreted by influenza A virus-infected macrophages are able to induce
IFN- synthesis in human T cells. Influenza A virus-infected human
peripheral macrophages secreted IFN-
/ß, TNF-, IL-1ß, and a
recently identified cytokine, IL-18 (or IFN--inducing factor),
whereas the production of IL-12 was not detected. Supernatants
collected from virus-infected macrophages induced rapid IFN- mRNA
expression and protein production in T cells. This was down-regulated
by the addition of neutralizing anti-IFN-/ß Abs, whereas
neutralizing anti-IL-12 Abs had no effect on IFN- gene
expression. Exogenously added IFN-/ß also rapidly stimulated the
synthesis of IFN- mRNA in T cells independently of protein
synthesis. IL-18 synergized with IFN- to up-regulate IFN- gene
expression and protein production. The data suggest that IFN-/ß
and IL-18 produced by macrophages during virus infection may act
together to induce IFN- synthesis and, consequently, may play an
important role for both of these cytokines in the development of
Th1-type immune responses.
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M. Miettinen, S. Matikainen, J. Vuopio-Varkila, J. Pirhonen, K. Varkila, M. Kurimoto, and I. Julkunen Lactobacilli and Streptococci Induce Interleukin-12 (IL-12), IL-18, and Gamma Interferon Production in Human Peripheral Blood Mononuclear Cells Infect. Immun., December 1, 1998; 66(12): 6058 - 6062. [Abstract] [Full Text] [PDF]
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