Abstract
Molecular mimicry between infectious agents and normal human host cell proteins represents one of the possible mechanisms responsible for autoimmunity. Among infectious agents, human cytomegalovirus (HCMV) is an ideal candidate for involvement in autoimmune disorders because of its lifelong persistence through periods of reactivation and latency and because of the extensive manipulation of innate and adaptive immunity. HCMV has been implicated in the pathogenesis of vascular damage in systemic sclerosis (SSc) and atherosclerosis. Based on our data, which demonstrate a cause-and-effect relationship between HCMV and endothelial cell aggression in SSc and atherosclerosis, we propose that immune responses to particular HCMV proteins may result in autoaggression through a mechanism of molecular mimicry of normally expressed endothelial cell surface molecules.
Original language | English |
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Pages (from-to) | 419-432 |
Number of pages | 14 |
Journal | Lupus |
Volume | 24 |
DOIs | |
Publication status | Published - Apr 25 2015 |
Keywords
- atherosclerosis
- autoimmune response
- endothelial cells
- HCMV
- systemic sclerosis
ASJC Scopus subject areas
- Rheumatology
- Medicine(all)