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Rapid Communication | Open Access

Spontaneous NETosis and type Ⅰ IFN signaling activation in resting neutrophils of chronic granulomatous disease patients with CYBB mutations

Zhengjing LuaWenjun MouaJianxin HebXuedong GecXiaolin Wanga( )Jingang Guia( )
Laboratory of Tumor Immunology, Key Laboratory of Major Diseases in Children, Ministry of Education, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing 100045, China
Department of Respiratory Medicine, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, China National Clinical Research Center for Respiratory Diseases, Beijing 100045, China
Information Center, PLA Rocket Force Characteristic Medical Center, Beijing 100088, China

Peer review under responsibility of Chongqing Medical University.

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References

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Roos DX, CGDbase. A database of X-CGD-causing mutations. Immunol Today. 1996;17(11):517–521.

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Lood C, Blanco LP, Purmalek MM, et al. Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease. Nat Med. 2016;22(2):146–153.

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Lee KH, Kronbichler A, Park DDY, et al. Neutrophil extracellular traps (NETs) in autoimmune diseases: a comprehensive review. Autoimmun Rev. 2017;16(11):1160–1173.

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Pylaeva E, Bordbari S, Spyra I, et al. Detrimental effect of type Ⅰ IFNs during acute lung infection with Pseudomonas aeruginosa is mediated through the stimulation of neutrophil NETosis. Front Immunol. 2019;10:2190.

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Kelkka T, Kienhöfer D, Hoffmann M, et al. Reactive oxygen species deficiency induces autoimmunity with type 1 interferon signature. Antioxidants Redox Signal. 2014;21(16):2231–2245.

Genes & Diseases
Article number: 101118
Cite this article:
Lu Z, Mou W, He J, et al. Spontaneous NETosis and type Ⅰ IFN signaling activation in resting neutrophils of chronic granulomatous disease patients with CYBB mutations. Genes & Diseases, 2024, 11(6): 101118. https://doi.org/10.1016/j.gendis.2023.101118

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Received: 29 May 2023
Published: 20 September 2023
© 2023 The Authors.

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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