Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 901 - 907 |
| Number of pages | 7 |
| Journal | Nature Immunology |
| Volume | 14 |
| Issue number | 9 |
| DOIs | |
| Publication status | Published - 2013 |
Cite this
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Structural basis of a unique interferon-beta signaling axis mediated via the receptor IFNAR1. / De Weerd, Nicole Anne; Vivian, Julian; Nguyen, Thao K; Mangan, Niamh; Gould, Jodee Ann; Braniff, Susie-Jane; Zaker-Tabrizi, Leyla; Fung, Ka Yee; Forster, Samuel; Beddoe, Travis Clarke; Reid, Hugh Harrington; Rossjohn, Jamie; Hertzog, Paul John.
In: Nature Immunology, Vol. 14, No. 9, 2013, p. 901 - 907.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Structural basis of a unique interferon-beta signaling axis mediated via the receptor IFNAR1
AU - De Weerd, Nicole Anne
AU - Vivian, Julian
AU - Nguyen, Thao K
AU - Mangan, Niamh
AU - Gould, Jodee Ann
AU - Braniff, Susie-Jane
AU - Zaker-Tabrizi, Leyla
AU - Fung, Ka Yee
AU - Forster, Samuel
AU - Beddoe, Travis Clarke
AU - Reid, Hugh Harrington
AU - Rossjohn, Jamie
AU - Hertzog, Paul John
PY - 2013
Y1 - 2013
N2 - 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.
AB - 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.
UR - http://www.nature.com/ni/journal/v14/n9/pdf/ni.2667.pdf
U2 - 10.1038/ni.2667
DO - 10.1038/ni.2667
M3 - Article
VL - 14
SP - 901
EP - 907
JO - Nature Immunology
JF - Nature Immunology
SN - 1529-2908
IS - 9
ER -