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• W1927991005 endingPage "5482" @default.
• W1927991005 startingPage "5477" @default.
• W1927991005 abstract "Abstract The IL-1 family member 7b (IL-1F7b) is a novel homolog of the IL-1 cytokine family discovered by computational cloning. We have reported that IL-1F7b shares critical amino acid residues with IL-18 and binds the IL-18-binding protein; in doing so, IL-1F7b augments the inhibition of IFN-γ by the IL-18-binding protein. IL-1F7b also binds IL-18Rα but neither induces signal nor acts as a receptor antagonist. Hence, the function of IL-1F7b remains unknown. In the present study, we analyzed the intracellular expression pattern of IL-1F7b. Using two variants of GFP fusion constructs of human IL-1F7b stably expressed in RAW macrophages, only the postcleavage mature form of the IL-1F7b precursor—but not the N-terminal propiece—specifically translocates to the nucleus following LPS stimulation. IL-1F7b, like IL-1β, IL-18, and IL-33, is processed by caspase-1 to generate the mature cytokines. Therefore, we tested whether caspase-1-mediated cleavage of the IL-1F7b precursor is required for mature IL-1F7b to translocate actively into the nucleus. Indeed, a specific caspase-1 inhibitor markedly reduced nuclear entry of IL-1F7b. In stable transfectants of human IL-1F7b in RAW macrophages stimulated with LPS, levels of TNF-α, IL-1α, IL-6, as well as the chemokine MIP-2, were substantially reduced (72–98%) compared with LPS-stimulated cells transfected with the empty plasmid. These results demonstrate that IL-1F7b translocates to the nucleus after caspase-1 processing and may act as a transcriptional modulator reducing the production of LPS-stimulated proinflammatory cytokines, consistent with IL-1F7b being an anti-inflammatory member of the IL-1 family." @default.
• W1927991005 created "2016-06-24" @default.
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• W1927991005 date "2008-04-15" @default.
• W1927991005 modified "2023-10-10" @default.
• W1927991005 title "The IL-1 Family Member 7b Translocates to the Nucleus and Down-Regulates Proinflammatory Cytokines" @default.
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• W1927991005 doi "https://doi.org/10.4049/jimmunol.180.8.5477" @default.
• W1927991005 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18390730" @default.
• W1927991005 hasPublicationYear "2008" @default.
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