First Author | Kopf M | Year | 1994 |
Journal | Nature | Volume | 368 |
Issue | 6469 | Pages | 339-42 |
PubMed ID | 8127368 | Mgi Jnum | J:17360 |
Mgi Id | MGI:65407 | Doi | 10.1038/368339a0 |
Citation | Kopf M, et al. (1994) Impaired immune and acute-phase responses in interleukin-6-deficient mice. Nature 368(6469):339-42 |
abstractText | Interleukin-6 (IL-6) is a multifunctional cytokine that regulates various aspects of the immune response, acute-phase reaction and haematopoiesis (for reviews see refs 1, 2). In vitro, leukaemia inhibitory factor, oncostatin M, ciliary neurotrophic factor and interleukin-11 display overlapping activities with IL-6. This functional redundancy may be explained by the interactions of specific binding receptors with a common signal-transducing receptor (gp130) (for reviews see refs 3, 4). To elucidate the unique function of IL-6 in vivo, we have disrupted the IL-6 gene by homologous recombination. IL-6-deficient mice develop normally. They fail to control efficiently vaccinia virus and infection with Listeria monocytogenes, a facultative intracellular bacterium. The T-cell-dependent antibody response against vesicular stomatitis virus is impaired. Further, the inflammatory acute-phase response after tissue damage or infection is severely compromised, whereas it is only moderately affected after challenge with lipopolysaccharide. We conclude that IL-6 production induced by injury or infection is an important in vivo SOS signal which coordinates activities of liver cells, macrophages and lymphocytes. |