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• W1549643265 abstract "Sluggish was identified in a population of third generation mice descended from N-ethyl-N-nitrosourea-mutagenized sires. Macrophages from homozygotes exhibited impaired TNF-alpha production in response to all TLR ligands tested and displayed impaired type I IFN production in response to TLR7 and TLR9 stimulations. The phenotype was confined to a critical region on mouse chromosome 18 and then ascribed to a T to A transversion in the acceptor splice site of intron 4 at position 13346 of the Map3k8 gene, resulting in defective splicing. The Map3k8(Sluggish) mutation does not result in susceptibility to viral infections, but Sluggish mice displayed high susceptibility to group B streptococcus infection, with impaired TNF-alpha and type I IFN production in infected macrophages. Our data demonstrate that the encoded protein kinase Tpl2 plays an essential role in cell signaling in the immune response to certain pathogens." @default.
• W1549643265 created "2016-06-24" @default.
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• W1549643265 date "2009-12-15" @default.
• W1549643265 modified "2023-09-27" @default.
• W1549643265 title "The Tpl2 Mutation <i>Sluggish</i> Impairs Type I IFN Production and Increases Susceptibility to Group B Streptococcal Disease" @default.
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• W1549643265 doi "https://doi.org/10.4049/jimmunol.0902718" @default.
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