Schattner A
Department of Medicine, Kaplan Hospital, Rehovot, Israel.
Isr J Med Sci. 1988 Dec;24(12):728-31.
All healthy subjects have the capacity to produce autoantibodies markedly similar to those seen in autoimmune disease. This capacity may be activated by viruses, through the release of IFN or other mechanisms. Autoimmune disease can be induced or enhanced by interferons in mice and in humans. Circulating IFNs are very frequent in patients with autoimmune diseases and may participate in the mediation of several clinical and immunologic manifestations. IFN-induced aberrant HLA-DR expression is common on epithelial cells of target organs of many autoimmune diseases; it may present autoantigen to T-cells and initiate a cycle of self-perpetuating autoimmunity. Interaction of IFN with other lymphokines (TNF, interleukin 1, etc.) may contribute to disease development. Further understanding of the role of lymphokines in autoimmunity may provide the basis for specific therapy in the future.
所有健康受试者都有能力产生与自身免疫性疾病中所见极为相似的自身抗体。这种能力可能由病毒通过释放干扰素或其他机制激活。在小鼠和人类中，干扰素可诱导或加重自身免疫性疾病。自身免疫性疾病患者中循环干扰素非常常见，可能参与多种临床和免疫表现的介导。干扰素诱导的异常HLA - DR表达在许多自身免疫性疾病靶器官的上皮细胞中很常见；它可能将自身抗原呈递给T细胞并启动一个自我持续的自身免疫循环。干扰素与其他淋巴因子（肿瘤坏死因子、白细胞介素1等）的相互作用可能有助于疾病发展。对淋巴因子在自身免疫中作用的进一步了解可能为未来的特异性治疗提供基础。
