Gharavi A E, Pierangeli S S, Harris E N
Department of Medicine, Morehouse School of Medicine, Atlanta, Georgia, USA.
Rheum Dis Clin North Am. 2001 Aug;27(3):551-63. doi: 10.1016/s0889-857x(05)70219-2.
Our observations and those from others give further support to our hypothesis that "autoimmune aPL" may be generated by immunization with products from bacteria or viruses after incidental exposure or infection. We also were able to generate an APS-like syndrome in a strain of mice susceptible to autoimmunity, indicating that other factors such as genetic factors are likely to be involved in development of APS. Furthermore, not all aPL generated by immunization with bacterial or viral products were pathogenic. Based on the clinical experience and on the numerous reports indicating the presence of aPL in large number of infectious diseases, it may be expected that not all aPL produced during infection are pathogenic. We hypothesize that a limited number aPL induced by certain viral or bacterial products would be pathogenic in certain groups of predisposed individuals. Identification of those bacterial or viral agents may help to find strategies for the prevention of production of "pathogenic" aPL. Alternatively, free peptides may be used to induce tolerance against aPL production.
我们的观察结果以及其他人的观察结果进一步支持了我们的假说，即“自身免疫性抗磷脂抗体”可能是在偶然接触或感染后，由细菌或病毒产物免疫产生的。我们还能够在一种易患自身免疫性疾病的小鼠品系中诱发类似抗磷脂综合征的症状，这表明其他因素如遗传因素可能参与了抗磷脂综合征的发病过程。此外，并非所有由细菌或病毒产物免疫产生的抗磷脂抗体都具有致病性。基于临床经验以及众多表明大量传染病中存在抗磷脂抗体的报告，可以预期并非所有感染期间产生的抗磷脂抗体都具有致病性。我们推测，某些病毒或细菌产物诱导产生的有限数量的抗磷脂抗体，在某些易感个体群体中可能具有致病性。识别这些细菌或病毒因子可能有助于找到预防“致病性”抗磷脂抗体产生的策略。或者，游离肽可用于诱导针对抗磷脂抗体产生的耐受性。
