The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Detection of interferon alpha protein reveals differential levels and cellular sources in disease
Open accessAbstract
Type I interferons (IFNs) are essential mediators of antiviral responses. These cytokines have been implicated in the pathogenesis of autoimmunity, most notably systemic lupus erythematosus (SLE), diabetes mellitus, and dermatomyositis, as well as monogenic type I interferonopathies. Despite a fundamental role in health and disease, the direct quantification of type I IFNs has been challenging. Using single-molecule array (Simoa) digital ELISA technology, we recorded attomolar concentrations of IFNα in healthy donors, viral infection, and complex and monogenic interferonopathies. IFNα protein correlated well with functional activity and IFN-stimulated gene expression. High circulating IFNα levels were associated with increased clinical severity in SLE patients, and a study of the cellular source of IFNα protein indicated disease-specific mechanisms. Measurement of IFNα attomolar concentrations by digital ELISA will enhance our understanding of IFN biology and potentially improve the diagnosis and stratification of pathologies associated with IFN dysregulation.
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Cites
Virus interference. I. the interferon
Isaacs, A., & Lindenmann, J. (1957) · Proceedings of the Royal Society of London. Series B - Biological Sciences · doi:10.1098/rspb.1957.0048 · Cited by 3,451
The Nature of the Principal Type 1 Interferon-Producing Cells in Human Blood
Siegal, F. P., Kadowaki, N., Shodell, M., Fitzgerald-Bocarsly, P. A., Shah, K., Ho, S., Antonenko, S., & Liu, Y.-J. (1999) · Science · doi:10.1126/science.284.5421.1835 · Cited by 2,293
Rissin, D. M., Kan, C. W., Campbell, T. G., Howes, S. C., Fournier, D. R., Song, L., Piech, T., Patel, P. P., Chang, L., Rivnak, A. J., et al. (2010) · Nature Biotechnology · doi:10.1038/nbt.1641 · Cited by 2,119
Self-citationImmune Interferon in the Circulation of Patients with Autoimmune Disease
Hooks, J. J., Moutsopoulos, H. M., Geis, S. A., Stahl, N. I., Decker, J. L., & Notkins, A. L. (1979) · New England Journal of Medicine · doi:10.1056/nejm197907053010102 · Cited by 921
Interferon‐α/β–mediated innate immune mechanisms in dermatomyositis
Greenberg, S. A., Pinkus, J. L., Pinkus, G. S., Burleson, T., Sanoudou, D., Tawil, R., Barohn, R. J., Saperstein, D. S., Briemberg, H. R., Ericsson, M., et al. (2005) · Annals of Neurology · doi:10.1002/ana.20464 · Cited by 621
Isaacs, A., & Lindenmann, J. (2015) · The Journal of Immunology · doi:10.1093/jimmunol/195.5.1911 · Cited by 602
Wilson, D. H., Rissin, D. M., Kan, C. W., Fournier, D. R., Piech, T., Campbell, T. G., Meyer, R. E., Fishburn, M. W., Cabrera, C., Patel, P. P., et al. (2016) · SLAS Technology · doi:10.1177/2211068215589580 · Cited by 470
Self-citationRice, G. I., Forte, G. M. A., Szynkiewicz, M., Chase, D. S., Aeby, A., Abdel-Hamid, M. S., Ackroyd, S., Allcock, R., Bailey, K. M., Balottin, U., et al. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(13)70258-8 · Cited by 443
Self-citationRodero, M. P., & Crow, Y. J. (2016) · Journal of Experimental Medicine · doi:10.1084/jem.20161596 · Cited by 433
Self-citationVirus interference. II. Some properties of interferon
Isaacs, A., Lindenmann, J., & Valentine, R. C. (1957) · Proceedings of the Royal Society of London. Series B - Biological Sciences · doi:10.1098/rspb.1957.0049 · Cited by 413
Cited by
Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients
Hadjadj, J., Yatim, N., Barnabei, L., Corneau, A., Boussier, J., Smith, N., Péré, H., Charbit, B., Bondet, V., Chenevier-Gobeaux, C., et al. (2020) · Science · doi:10.1126/science.abc6027 · Cited by 2,984
Self-citationMitochondrial double-stranded RNA triggers antiviral signalling in humans
Dhir, A., Dhir, S., Borowski, L. S., Jimenez, L., Teitell, M., Rötig, A., Crow, Y. J., Rice, G. I., Duffy, D., Tamby, C., et al. (2018) · Nature · doi:10.1038/s41586-018-0363-0 · Cited by 631
Self-citationHuman ADAR1 Prevents Endogenous RNA from Triggering Translational Shutdown
Chung, H., Calis, J. J. A., Wu, X., Sun, T., Yu, Y., Sarbanes, S. L., Dao Thi, V. L., Shilvock, A. R., Hoffmann, H.-H., Rosenberg, B. R., et al. (2018) · Cell · doi:10.1016/j.cell.2017.12.038 · Cited by 538
The type I interferonopathies: 10 years on
Crow, Y. J., & Stetson, D. B. (2022) · Nature Reviews Immunology · doi:10.1038/s41577-021-00633-9 · Cited by 489
Self-citationReverse-Transcriptase Inhibitors in the Aicardi–Goutières Syndrome
Rice, G. I., Meyzer, C., Bouazza, N., Hully, M., Boddaert, N., Semeraro, M., Zeef, L. A. H., Rozenberg, F., Bondet, V., Duffy, D., et al. (2018) · New England Journal of Medicine · doi:10.1056/nejmc1810983 · Cited by 153
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Metadata
- Authors
- Rodero, M. P., Decalf, J., Bondet, V., Hunt, D., Rice, G. I., Werneke, S., McGlasson, S. L., Alyanakian, M.-A., Bader-Meunier, B., Barnerias, C., Bellon, N., Belot, A., Bodemer, C., Briggs, T. A., Desguerre, I., Frémond, M.-L., Hully, M., van den Maagdenberg, A. M. J. M., Melki, I., Meyts, I., Musset, L., Pelzer, N., Quartier, P., Terwindt, G. M., Wardlaw, J., Wiseman, S., Rieux-Laucat, F., Rose, Y., Neven, B., Hertel, C., Hayday, A., Albert, M. L., Rozenberg, F., Crow, Y. J., & Duffy, D.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2017-04-18
- Volume
- 214
- Issue
- 5
- Pages
- 1547-1555
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2606492431
- Cited by
- 375
- References
- 23
- FWCI
- 15.28
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Rodero, M. P., Decalf, J., Bondet, V., Hunt, D., Rice, G. I., Werneke, S., McGlasson, S. L., Alyanakian, M.-A., Bader-Meunier, B., Barnerias, C., Bellon, N., Belot, A., Bodemer, C., Briggs, T. A., Desguerre, I., Frémond, M.-L., Hully, M., van den Maagdenberg, A. M. J. M., Melki, I., . . . Duffy, D. (2017). Detection of interferon alpha protein reveals differential levels and cellular sources in disease. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20161451
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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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