Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Bonder, C.S. et al.

Endogenous interferon-alpha production by differentiating human monocytes regulates expression and function of the IL-2/IL-4 receptor gamma chain.

In vitro monocyte-derived macrophages (MDMac) and synovial fluid macrophages from inflamed joints differ from monocytes in their responses to interleukin 4 (IL-4). While IL-4 can suppress LPS- induced interleukin beta (IL-beta) and tumour necrosis factor alpha (TNF-alpha) production by monocytes, IL-4 can suppress LPS- induced IL-1 beta, but not TNFalpha production by the more differentiated cells. Recently we reported a correlation between the ability of IL-4 to regulate TNFalpha production by monocytes and the expression of the IL-4 receptor gamma chain or gamma common (gamma c chain). Like MDMac, interferon alpha (IFNalpha)-treated monocytes expressed less IL-4 receptor gamma c chain, reduced levels of IL-4- activated STAT6 and IL-4 could not suppress LPS-induced TNFalpha production. In addition, like monocytes and MDMac, IFNalpha-treated monocytes expressed normal levels of the IL-4 receptor alpha chain and IL-4 significantly suppressed LPS- induced IL-1 beta production. With addition of IFNalpha-neutralizing antibodies, the ability of IL-4 to suppress LPS-induced TNFalpha production with prolonged monocyte culture was restored. Detection of IFNalpha in synovial fluids from inflamed joints further implicates IFNalpha in the inability of IL-4 to suppress TNFalpha production by synovial fluid macrophages. This study identifies a mechanism for the differential expression of gamma c and varied responses to IL-4 by human monocytes compared with MDMac.[1]

References

Endogenous interferon-alpha production by differentiating human monocytes regulates expression and function of the IL-2/IL-4 receptor gamma chain. Bonder, C.S., Davies, K.V., Liu, X., Hertzog, P.J., Woodcock, J.M., Finlay-Jones, J.J., Hart, P.H. Cytokine (2002) [Pubmed]

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