Steinberg A D, Raveché E S, Laskin C A, Smith H R, Santoro T, Miller M L, Plotz P H
Ann Intern Med. 1984 May;100(5):714-27. doi: 10.7326/0003-4819-100-5-714.
Systemic lupus erythematosus is a multisystem, antibody-mediated, autoimmune disorder that occurs spontaneously in humans and mice. Genetic factors appear to play an important predisposing role in the disorder: The presence of certain genes may produce a generalized immune abnormality, whereas others may lead to specific autoantibodies. Environmental triggers increase autoantibody production and augment the expression of illness. Bacterial and viral illnesses can provide stimulation by activating macrophages and T cells that, in turn, stimulate B cells. In the absence of normal control mechanisms, the stimulatory process is not suppressed, and excessive stem cell proliferation results in abnormal B-cell proliferation. A trigger for the disease is the signaling of the proliferating B cells to differentiate into antibody-forming cells. Most autoantibody-producing B cells can be eliminated from mice with lupus erythematosus by virtue of the presence of the gene, xid. In addition, administration of an analog of arachidonic acid is an effective treatment for murine lupus erythematosus.
系统性红斑狼疮是一种多系统、抗体介导的自身免疫性疾病，可在人类和小鼠中自发发生。遗传因素似乎在该疾病中起着重要的易患作用：某些基因的存在可能会产生全身性免疫异常，而其他基因可能会导致特定的自身抗体。环境触发因素会增加自身抗体的产生并加剧疾病的表现。细菌和病毒感染可通过激活巨噬细胞和T细胞来提供刺激，进而刺激B细胞。在缺乏正常控制机制的情况下，刺激过程不会受到抑制，干细胞过度增殖会导致B细胞异常增殖。该疾病的一个触发因素是增殖的B细胞分化为抗体形成细胞的信号。由于存在xid基因，大多数产生自身抗体的B细胞可以从小鼠的红斑狼疮中消除。此外，给予花生四烯酸类似物是治疗小鼠红斑狼疮的有效方法。
