Hang L, Slack J H, Amundson C, Izui S, Theofilopoulos A N, Dixon F J
J Exp Med. 1983 Mar 1;157(3):874-83. doi: 10.1084/jem.157.3.874.
In vivo, prolonged polyclonal activation of B cells by the nonantigenic but potent mitogenic lipid A portion of lipopolysaccharide (LPS-R595) resulted in acceleration of the late life systemic lupus erythematosus disease of female MRL/n, BXSB, and NZW mice, mimicking the time, form, and histopathological features characteristic of their early life disease counterparts, i.e., MRL/l females, BXSB males, and (NZB X NZW)F1 females. Similar polyclonal B cell activation of "immunologically normal" mice has less effect and led to a limited expression of autoimmune disease. This R595-induced autoimmunity and immune complex-mediated disease seemed to be the direct result of activation of the immune system and not from other effects of endotoxin since C3H/HeJ, a strain lacking lymphocyte receptors for LPS-R595, had neither serological nor histological evidence of autoimmune disease despite identical treatment.
在体内，脂多糖（LPS-R595）的非抗原性但具有强促有丝分裂作用的脂质A部分对B细胞进行长时间多克隆激活，导致雌性MRL/n、BXSB和NZW小鼠的晚期系统性红斑狼疮疾病加速，模拟了其早期疾病对应物（即MRL/l雌性、BXSB雄性和（NZB×NZW）F1雌性）的时间、形式和组织病理学特征。对“免疫正常”小鼠进行类似的多克隆B细胞激活作用较小，并导致自身免疫疾病的有限表达。这种R595诱导的自身免疫和免疫复合物介导的疾病似乎是免疫系统激活的直接结果，而非内毒素的其他作用，因为缺乏LPS-R595淋巴细胞受体的C3H/HeJ品系，尽管接受了相同处理，但既没有自身免疫疾病的血清学证据，也没有组织学证据。
