Molecular mimicry between infectious agents and normal human host cell components is one of the mechanisms responsible for autoimmunity. Among infectious agents, some viruses represent ideal candidates for their ability to infect human cells, where they are harbored for the duration of the life of the host in a latent state. Human cytomegalovirus (hCMV) infection has been implicated in the pathogenesis of vascular damage in systemic sclerosis (SSc) and atherosclerosis. Based on recent data describing a cause and effect relationship between hCMV and endothelial cell damage in SSc and atherosclerosis, we propose that the immune response to particular hCMV proteins might result in autoaggression through a mechanism of molecular mimicry of normally expressed endothelial cell surface molecules.
Induction of endothelial cell damage by hCMV molecular mimicry
LUNARDI, Claudio;BASON, Caterina;CORROCHER, Roberto;
2005-01-01
Abstract
Molecular mimicry between infectious agents and normal human host cell components is one of the mechanisms responsible for autoimmunity. Among infectious agents, some viruses represent ideal candidates for their ability to infect human cells, where they are harbored for the duration of the life of the host in a latent state. Human cytomegalovirus (hCMV) infection has been implicated in the pathogenesis of vascular damage in systemic sclerosis (SSc) and atherosclerosis. Based on recent data describing a cause and effect relationship between hCMV and endothelial cell damage in SSc and atherosclerosis, we propose that the immune response to particular hCMV proteins might result in autoaggression through a mechanism of molecular mimicry of normally expressed endothelial cell surface molecules.
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