发病机制
免疫学
免疫系统
医学
机制(生物学)
疾病
系统性红斑狼疮
基因
细胞因子
遗传倾向
红斑狼疮
生物
遗传学
抗体
病理
哲学
认识论
作者
Jessica Manson,David Isenberg
出处
期刊:Springer eBooks
[Springer Nature]
日期:2021-01-01
被引量:75
标识
DOI:10.1007/978-3-030-85161-3
摘要
SLE is a complex, heterogeneous disease, the precise pathogenesis of which remains something of a mystery. In recent years our understanding has been advanced by the development of novel genetic and immunological techniques. Susceptibility to SLE has a genetic component and multiple putative genes are being investigated. The genes involved are likely to play a part in immune regulation. Central to the immune dysfunction seen in SLE is the presence of autoreactive B cells, which predominantly target nuclear antigens. In addition to evidence of aberrant B and T cell behaviour, lupus is associated with complement deficiencies, and abnormal cytokine function. A number of environmental triggers exist, and likely candidates include viral infection and exposure to UV light. Finally, evidence is accumulating that implicates apoptosis as a mechanism by which disease may be provoked and propagated.
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