Eros is a novel transmembrane protein that controls the phagocyte respiratory burst and is essential for innate immunityReportar como inadecuado


Eros is a novel transmembrane protein that controls the phagocyte respiratory burst and is essential for innate immunity


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Publication Date: 2017-04-03

Journal Title: The Journal of Experimental Medicine

Publisher: Rockefeller University Press

Volume: 214

Issue: 4

Pages: 1111-1128

Language: English

Type: Article

This Version: VoR

Metadata: Show full item record

Citation: Thomas, D., Clare, S., Sowerby, J. M., Pardo, M., Juss, J., Goulding, D., van der Weyden, L., et al. (2017). Eros is a novel transmembrane protein that controls the phagocyte respiratory burst and is essential for innate immunity. The Journal of Experimental Medicine, 214 (4), 1111-1128. https://doi.org/10.1084/jem.20161382

Abstract: The phagocyte respiratory burst is crucial for innate immunity. The transfer of electrons to oxygen is mediated by a membrane-bound heterodimer, comprising gp91$\textit{phox}$ and p22$\textit{phox}$ subunits. Deficiency of either subunit leads to severe immunodeficiency. We describe Eros (essential for reactive oxygen species), a protein encoded by the previously undefined mouse gene $\textit{bc017643}$, and show that it is essential for host defense via the phagocyte NAPDH oxidase. Eros is required for expression of the NADPH oxidase components, gp91$\textit{phox}$ and p22$\textit{phox}$. Consequently, $\textit{Eros}$-deficient mice quickly succumb to infection. $\textit{Eros}$ also contributes to the formation of neutrophil extracellular traps (NETS) and impacts on the immune response to melanoma metastases. $\textit{Eros}$ is an ortholog of the plant protein Ycf4, which is necessary for expression of proteins of the photosynthetic photosystem 1 complex, itself also an NADPH oxio-reductase. We thus describe the key role of the previously uncharacterized protein Eros in host defense.

Sponsorship: D.C. Thomas was funded by a Wellcome Trust/CIMR Next Generation Fellowship, a National Institute for Health Research (NIHR) Clinical Lectureship, and a Starter Grant for Clinical Lecturers (Academy of Medical Sciences). K.G.C. Smith was funded by funded by the Medical Research Council (program grant MR/L019027) and is a Wellcome Investigator and a NIHR Senior Investigator. S. Clare and G. Dougan were funded by the Wellcome Trust (grant 098051). The Cambridge Institute for Medical Research is in receipt of a Wellcome Trust Strategic Award (079895). J.C.L is funded by a Wellcome Intermediate Clinical Fellowship 105920/2/14/2.

Identifiers:

External DOI: https://doi.org/10.1084/jem.20161382

This record's URL: https://www.repository.cam.ac.uk/handle/1810/263481



Rights: Attribution 4.0 International

Licence URL: http://creativecommons.org/licenses/by/4.0/





Autor: Thomas, DCClare, SSowerby, John MartinPardo, MJuss, JKGoulding, DAvan der Weyden, LStoristeanu, DPrakash, AEspéli, MFlint, S Lee,

Fuente: https://www.repository.cam.ac.uk/handle/1810/263481



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