학술논문
The roles of tumour necrosis factor-α, interleukin-1 and interleukin-12 in murine cytomegalovirus infection.
Document Type
Article
Source
Subject
*IMMUNOGLOBULINS
*TUMOR necrosis factors
*MACROPHAGES
*GROWTH factors
*GLYCOPROTEINS
*CYTOMEGALOVIRUSES
*IMMUNITY
*IMMUNOLOGY
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Language
ISSN
0019-2805
Abstract
The roles of the inflammatory cytokines tumour necrosis factor-α (TNF-α), interleukin-1 (IL-1) and IL-12, in murine cytomegalovirus (MCMV) disease were investigated in susceptible BALB/c and resistant C57BL/6 mice. MCMV infection induced IL-1 and TNF-α production by peritoneal cells from BALB/c mice, as demonstrated previously in C57BL/6 mice. Overt ill-health and viral replication in the spleens of BALB/c mice were increased by in vivo treatment with soluble TNFα receptors to inhibit the activity of this cytokine, whilst antibodies to IL-12 had a similar but more restricted effect. C57BL/6 mice were not affected by either treatment, suggesting TNF-α and IL-12 are not critical for natural killer cell-mediated restriction of viral replication in the spleen. Soluble TNF-α receptors and antibodies to IL-12 also enhanced MCMV titres and numbers of viral antigen-positive cells in the livers of BALB/c mice and TNF-α receptors have similar effects in C57BL/6 livers. In contrast, IL-1 receptors improved the health of MCMV-infected BALB/c mice and reduced viral replication and hepatitis at some time-points. Mechanisms which may underlie these changes are discussed. [ABSTRACT FROM AUTHOR]