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dc.contributor.authorMarino Gammazza, Antonella
dc.contributor.authorLégaré, Sébastien
dc.contributor.authorLo Bosco, Giosuè
dc.contributor.authorFucarino, Alberto
dc.contributor.authorAngileri, Francesca
dc.contributor.authorConway de Macario, Everly
dc.contributor.authorMacario, Alberto Jl
dc.contributor.authorCappello, Francesco
dc.date.accessioned2020-08-17T17:54:01Z
dc.date.available2020-08-17T17:54:01Z
dc.date.issued2020-08-04
dc.identifier.urihttp://hdl.handle.net/10713/13563
dc.description.abstractSevere acute respiratory syndrome corona virus 2 (SARS-CoV-2), the cause of COVID-19 disease, has the potential to elicit autoimmunity because mimicry of human molecular chaperones by viral proteins. We compared viral proteins with human molecular chaperones, many of which are heat shock proteins, to determine if they share amino acid-sequence segments with immunogenic-antigenic potential, which can elicit cross-reactive antibodies and effector immune cells with the capacity to damage-destroy human cells by a mechanism of autoimmunity. We identified the chaperones that can putatively participate in molecular mimicry phenomena after SARS-CoV-2 infection, focusing on those for which endothelial cell plasma-cell membrane localization has already been demonstrated. We also postulate that post-translational modifications, induced by physical (shear) and chemical (metabolic) stress caused respectively by the risk factors hypertension and diabetes, might have a role in determining plasma-cell membrane localization and, in turn, autoimmune-induced endothelial damage.en_US
dc.description.urihttps://doi.org/10.1007/s12192-020-01148-3en_US
dc.language.isoen_USen_US
dc.publisherSpringer Natureen_US
dc.relation.ispartofCell Stress and Chaperonesen_US
dc.subjectAutoimmunityen_US
dc.subjectCOVID-19en_US
dc.subjectEndothelialitisen_US
dc.subjectMolecular chaperonesen_US
dc.subjectMolecular mimicryen_US
dc.subjectSevere acute respiratory syndrome coronavirus 2en_US
dc.titleHuman molecular chaperones share with SARS-CoV-2 antigenic epitopes potentially capable of eliciting autoimmunity against endothelial cells: possible role of molecular mimicry in COVID-19en_US
dc.typeArticleen_US
dc.identifier.doi10.1007/s12192-020-01148-3
dc.identifier.scopusidSCOPUS_ID:85089069385


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