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SARS-CoV-2 immune complex triggers human monocyte necroptosis

We analyzed the ability of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) itself and SARS-CoV-2-IgG immune complexes to trigger human monocyte necroptosis. SARS-CoV-2 was able to induce monocyte necroptosis dependently of MLKL activation. Necroptosis-associated proteins (RIPK1, RIPK3 a...

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Detalles Bibliográficos
Autores principales: Santos, Leonardo Duarte, Antunes, Krist Helen, Cassão, Gisele, Gonçalves, João Ismael, Abbadi, Bruno Lopes, Bizarro, Cristiano Valim, Basso, Luiz Augusto, Machado, Pablo, de Souza, Ana Paula D., Porto, Bárbara Nery
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier B.V. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9968621/
https://www.ncbi.nlm.nih.gov/pubmed/36870284
http://dx.doi.org/10.1016/j.intimp.2023.109954
Descripción
Sumario:We analyzed the ability of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) itself and SARS-CoV-2-IgG immune complexes to trigger human monocyte necroptosis. SARS-CoV-2 was able to induce monocyte necroptosis dependently of MLKL activation. Necroptosis-associated proteins (RIPK1, RIPK3 and MLKL) were involved in SARS-CoV-2N1 gene expression in monocytes. SARS-CoV-2 immune complexes promoted monocyte necroptosis in a RIPK3- and MLKL-dependent manner, and Syk tyrosine kinase was necessary for SARS-CoV-2 immune complex-induced monocyte necroptosis, indicating the involvement of Fcγ receptors on necroptosis. Finally, we provide evidence that elevated LDH levels as a marker of lytic cell death are associated with COVID-19 pathogenesis.