期刊
NATURE IMMUNOLOGY
卷 14, 期 9, 页码 901-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2667
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资金
- National Health and Medical Research Council (NHMRC)
- The Australian Research Council (ARC)
- Victorian Government's Operational Infrastructure Support Program
- ARC Centre for Excellence in Structural and Functional Microbial Genomics
- ARC
- NHMRC
- Pfizer Australia Research Fellowship
- NHMRC Senior Principal Research fellowship
- NHMRC Australia Fellowship
Type I interferons are important in regulating immune responses to pathogens and tumors. All interferons are considered to signal via the heterodimeric IFNAR1-IFNAR2 complex, yet some subtypes such as interferon-beta ( IFN-beta) can exhibit distinct functional properties, although the molecular basis of this is unclear. Here we demonstrate IFN-beta can uniquely and specifically ligate to IFNAR1 in an IFNAR2-independent manner, and we provide the structural basis of the IFNAR1-IFN-beta interaction. The IFNAR1-IFN-beta complex transduced signals that modulated expression of a distinct set of genes independently of Jak-STAT pathways. Lipopolysaccharide-induced sepsis was ameliorated in Ifnar1(-/-) mice but not Ifnar2(-/-) mice, suggesting that IFNAR1-IFN-beta signaling is pathologically relevant. Thus, we provide a molecular basis for understanding specific functions of IFN-beta.
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