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抗DNA抗体的起源与致病性。

Genesis and pathogenicity of anti-DNA antibodies.

作者信息

Fournie G J, Izui S, Lambert P H, Conte J J

出版信息

Adv Nephrol Necker Hosp. 1976;6:47-61.

PMID:139082
Abstract

The formation of anti-DNA antibodies appears to be under a genetic control similar to that regulating the immune response to complex antigenic compounds. The ability to develop a high immune response to DNA seems to be predominantly dependent on the nature of the B-cell population whereas a major role of the T-cell suppressor population is not evident in this response. The immune response to DNA does not necessarily need the presence of thymus-derived lymphocytes, but in some cases T-cells may exert a helper effect. The development of anti-DNA antibody response may be triggered by various factors: viral, bacterial or parasitic agents, tissue destruction or some drugs. A mechanism that may play an important role is the "nonspecific" triggering of anti-DNA antibodies by substances that, like bacterial lipopolysaccharides, exert a potent stimulatory effect on B-cells and simultaneously induce a release of DNA in extracellular fluids. In lupus diseases as well as in mice injected with lipopolysaccharide, pathogenic effects of anti-DNA antibodies appear to be closely related to the formation of DNA-anti-DNA complexes. The demonstration that injections of lipopolysaccharide lead to the localization of DNA-anti-DNA complexes in kidney glomeruli stressed the possible importance of stimuli responsible for a release of DNA in circulating blood in the expression of the pathogenic effects of anti-DNA antibodies.

摘要

抗DNA抗体的形成似乎受一种与调节对复合抗原性化合物免疫反应相似的基因控制。对DNA产生高免疫反应的能力似乎主要取决于B细胞群体的性质,而在这种反应中T细胞抑制群体的主要作用并不明显。对DNA的免疫反应不一定需要胸腺来源的淋巴细胞存在,但在某些情况下T细胞可能发挥辅助作用。抗DNA抗体反应的发展可能由多种因素触发:病毒、细菌或寄生虫病原体、组织破坏或某些药物。一种可能起重要作用的机制是,像细菌脂多糖这样的物质对B细胞发挥强大的刺激作用并同时诱导细胞外液中DNA释放,从而“非特异性”触发抗DNA抗体。在狼疮疾病以及注射了脂多糖的小鼠中,抗DNA抗体的致病作用似乎与DNA-抗DNA复合物的形成密切相关。注射脂多糖会导致DNA-抗DNA复合物在肾小球中定位,这一证明强调了循环血液中负责DNA释放的刺激因素在抗DNA抗体致病作用表达中的可能重要性。

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