An etiopathogenic role for the type IIFN system in SLE

被引:162
作者
Rönnblom, L [1 ]
Alm, GV
机构
[1] Univ Uppsala Hosp, Dept Med Sci, Rheumatol Sect, S-75185 Uppsala, Sweden
[2] Biomed Ctr, Immunol Sect, Dept Vet Microbiol, S-75123 Uppsala, Sweden
关键词
D O I
10.1016/S1471-4906(01)01955-X
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The type I interferon (IFN) system plays a pivotal role in the etiopathogenesis of systemic lupus erythematosus (SLE). The initial appearance of autoantibody-producing B cells can be precipitated by infection-induced type IIFNs, but the further, significant generation of autoimmune T and B cells is caused by the prolonged production of IFN-a, which is maintained by a vicious circle mechanism. This involves the activation of immature dendritic cells, known as natural IFN-producing cells, by continuously formed endogenous IFN-alpha inducers. These IFN-a inducers consist of complexes of autoantibodies with nucleic-acid-containing autoantigens derived from apoptotic cells.
引用
收藏
页码:427 / 431
页数:5
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