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The B. Shine Department of Rheumatology, Rambam Medical Center, Haifa, Israel. a_rozin@rambam.health.gov.il
Very recently, several studies have convincingly demonstrated the role of infection in the development of the antiphospholipid syndrome. Cross antibody-mediated reactivity due to molecular mimicry between endothelial glycoproteins and microbial products was considered as an important pathogenic mechanism. However, another consequence of the molecular mimicry may be proposed. Similar tissues have less likelihood of being rejected and have a greater chance of being accepted by the host. According to this principle, pathogens with common-to-host antigens may attach readily and not be eliminated. A direct expansion of such pathogens may involve new territories. The targets of the approach 1, "from molecular mimicry to cross-reactivity," are T-B cells system inhibition-modulation. The targets of approach 2, "from molecular mimicry to pathogen expansion," are pathogens, enforcement of barriers, elimination techniques, and preventive strategy.
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