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Type 3 hypersensitivity in COVID-19 vasculitis

Coronavirus Disease 2019 (COVID-19) is an ongoing public health emergency and new knowledge about its immunopathogenic mechanisms is deemed necessary in the attempt to reduce the death burden, globally. For the first time in worldwide literature, we provide scientific evidence that in COVID-19 vascu...

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Detalles Bibliográficos
Autores principales: Roncati, Luca, Ligabue, Giulia, Fabbiani, Luca, Malagoli, Claudia, Gallo, Graziana, Lusenti, Beatrice, Nasillo, Vincenzo, Manenti, Antonio, Maiorana, Antonio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7256503/
https://www.ncbi.nlm.nih.gov/pubmed/32479986
http://dx.doi.org/10.1016/j.clim.2020.108487
Descripción
Sumario:Coronavirus Disease 2019 (COVID-19) is an ongoing public health emergency and new knowledge about its immunopathogenic mechanisms is deemed necessary in the attempt to reduce the death burden, globally. For the first time in worldwide literature, we provide scientific evidence that in COVID-19 vasculitis a life-threatening escalation from type 2 T-helper immune response (humoral immunity) to type 3 hypersensitivity (immune complex disease) takes place. The subsequent deposition of immune complexes inside the vascular walls is supposed to induce a severe inflammatory state and a cytokine release syndrome, whose interleukin-6 is the key myokine, from the smooth muscle cells of blood vessels.