Gharavi Azzudin E, Pierangeli Silvia S, Harris E Nigel
Dept. of Medicine, Morehouse School of Medicine, University of Atlanta, Atlanta Georgia 30310-1495, USA.
Immunobiology. 2003;207(1):37-42. doi: 10.1078/0171-2985-00216.
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 APS-like syndrome in a strain of mice susceptible to autoimmunity, indicating that other factors such as genetics are likely to be involved in the development of APS. Furthermore, not all aPL antibodies generated by immunization with bacterial or viral products are pathogenic. Based on the clinical experience and on the numerous reports indicating presence of aPL in a large number of infectious diseases, it may be expected that not all aPL antibodies produced during infection will be pathogenic. We hypothesize that a limited number aPL antibodies induced by certain viral/bacterial products would be pathogenic in certain groups of predisposed individuals. Identification of these bacterial and/ or viral agents may help to find strategies for the prevention of production of aPL "pathogenic" antibodies. 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设,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,这表明诸如遗传学等其他因素可能参与了抗磷脂综合征的发展。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是致病性的。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会具有致病性。我们假设,某些病毒/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会具有致病性。识别这些细菌和/或病毒因子可能有助于找到预防产生“致病性”抗磷脂抗体的策略。或者,游离肽可用于诱导对产生抗磷脂抗体的耐受性。