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Sergei V. Kotenko

Researcher at Rutgers University

Publications -  75
Citations -  7807

Sergei V. Kotenko is an academic researcher from Rutgers University. The author has contributed to research in topics: Receptor & Interferon. The author has an hindex of 33, co-authored 70 publications receiving 7088 citations. Previous affiliations of Sergei V. Kotenko include University of Medicine and Dentistry of New Jersey & Ruhr University Bochum.

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Journal ArticleDOI

Interferon-λ Mediates Non-redundant Front-Line Antiviral Protection against Influenza Virus Infection without Compromising Host Fitness.

TL;DR: Lambda interferons (IFN&lgr;s) or type III IFNs share homology, expression patterns, signaling cascades, and antiviral functions with type I IFNs, and are shown to provide front‐line antiviral protection without activating inflammation.
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Identification, Cloning, and Characterization of a Novel Soluble Receptor That Binds IL-22 and Neutralizes Its Activity

TL;DR: The addition of IL-22BP neutralizes the ability ofIL-22 to induce Stat activation and MHC class I Ag expression in these cells, and inhibits IL-21 activity by binding IL-23 and blocking its interaction with the cell surface IL- 22R complex.
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IFN Regulatory Factor Family Members Differentially Regulate the Expression of Type III IFN (IFN-λ) Genes

TL;DR: The data suggest that the IFN-λ1 gene is regulated by virus-activated IRF3 and IRF7, thus resembling that of the IFn-β gene, whereas IFN'sλ2/3 gene expression is mainly controlled by IRF 7, thus resembles those of IFN -α genes.
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Interleukin 24 (MDA-7/MOB-5) Signals through Two Heterodimeric Receptors, IL-22R1/IL-20R2 and IL-20R1/IL-20R2

TL;DR: It is shown that the human IL-24 is secreted by activated peripheral blood mononuclear cells and is the ligand for two heterodimeric receptors, IL-22R1/IL-20R2 and IL-20 R1/ IL- 20R2.
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Lambda Interferon Is the Predominant Interferon Induced by Influenza A Virus Infection In Vivo

TL;DR: It is demonstrated that intranasal influenza A virus infection leads to the robust type III IFN induction in the lungs of both WT and IFNAR−/− mice, consistent with previous studies showing thatIFNAR-mediated protection is redundant for mucosal influenza virus infection.