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Cited by 377

The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.

A null mutation in the gene encoding a type I interferon receptor component eliminates antiproliferative and antiviral responses to interferons alpha and beta and alters macrophage responses.

Open access
Hwang, S Y, Hertzog, P J, Holland, K A, Sumarsono, S H, Tymms, M J, Hamilton, J A, Whitty, G, Bertoncello, I, Kola, I·1995·Proceedings of the National Academy of Sciences

Abstract

To examine the in vivo role(s) of type I interferons (IFNs) and to determine the role of a component of the type I IFN receptor (IFNAR1) in mediating responses to these IFNs, we generated mice with a null mutation (-/-) in the IFNAR1 gene. Despite compelling evidence for modulation of cell proliferation and differentiation by type I IFNs, there were no gross signs of abnormal fetal development or morphological changes in adult IFNAR1-/- mice. However, abnormalities of hemopoietic cells were detected in IFNAR1 -/- mice. Elevated levels of myeloid lineage cells were detected in peripheral blood and bone marrow by staining with Mac-1 and Gr-1 antibodies. Furthermore, bone marrow macrophages from IFNAR1 -/- mice showed abnormal responses to colony-stimulating factor 1 and lipopolysaccharide. IFNAR1 -/- mice were highly susceptible to viral infection: viral titers were undetected 24 hr after infection of IFNAR1 +/+ mice but were extremely high in organs of IFNAR1 -/- mice, demonstrating that the type I IFN system is a major acute antiviral defence. In cell lines derived from IFNAR1 -/- mice, there was no signaling in response to IFN-alpha or -beta as measured by induction of 2'-5' oligoadenylate synthetase, antiviral, or antiproliferative responses. Importantly, these studies demonstrate that type I IFNs function in the development and responses of myeloid lineage cells, particularly macrophages, and that the IFNAR1 receptor component is essential for antiproliferative and antiviral responses to IFN-alpha and -beta.

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Metadata

Authors
Hwang, S. Y., Hertzog, P. J., Holland, K. A., Sumarsono, S. H., Tymms, M. J., Hamilton, J. A., Whitty, G., Bertoncello, I., & Kola, I.
Venue
Proceedings of the National Academy of Sciences
Published
1995-11-21
Volume
92
Issue
24
Pages
11284-11288
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W1968134447
Cited by
377
References
19
FWCI
3.46
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: A null mutation in the gene encoding a type I interferon receptor component eliminates antiproliferative and antiviral responses to interferons alpha and beta and alters macrophage responses. https://app.cochat.ai/papers/10.1073/pnas.92.24.11284
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Hwang, S. Y., Hertzog, P. J., Holland, K. A., Sumarsono, S. H., Tymms, M. J., Hamilton, J. A., Whitty, G., Bertoncello, I., & Kola, I. (1995). A null mutation in the gene encoding a type I interferon receptor component eliminates antiproliferative and antiviral responses to interferons alpha and beta and alters macrophage responses. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.92.24.11284

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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