Rozin Alexander P
The B. Shine Department of Rheumatology, Rambam Medical Center, Haifa, Israel.
Clin Rheumatol. 2007 Mar;26(3):285-8. doi: 10.1007/s10067-006-0352-9. Epub 2006 Jun 29.
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.
最近,多项研究令人信服地证明了感染在抗磷脂综合征发展中的作用。由于内皮糖蛋白与微生物产物之间的分子模拟导致的交叉抗体介导的反应性被认为是一种重要的致病机制。然而,分子模拟的另一个后果也值得一提。具有相似组织的物质被宿主排斥的可能性较小,被宿主接受的机会更大。根据这一原理,具有与宿主共同抗原的病原体可能容易附着且不会被清除。此类病原体的直接扩散可能会涉及新的领域。方法1“从分子模拟到交叉反应性”的目标是T-B细胞系统的抑制-调节。方法2“从分子模拟到病原体扩散”的目标是病原体、加强屏障、清除技术和预防策略。