Type I interferon in systemic lupus erythematosus and other autoimmune diseases

被引:768
作者
Banchereau, Jacques [1 ]
Pascual, Virginia [1 ]
机构
[1] Baylor Inst Immunol Res, Dallas, TX 75204 USA
关键词
D O I
10.1016/j.immuni.2006.08.010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Different genetic alterations may lead to type I interferon (IFN) overproduction in human systemic lupus erythematosus (SLE). The increased bioavailability of type I IFN contributes to peripheral tolerance breakdown through the activation of immature myeloid dendritic cells (mDCs). IFN-matured mDCs activate autoreactive T cells. These cells, together with plasmacytoid DCs, help expand autoreactive B cells. IFN-matured DCs also activate cytotoxic CD8(+) T cells, possibly increasing apoptotic cell availability. The capture of apoptotic cells by mDCs and of nucleic acid-containing immune complexes by plasmacytoid DCs and B cells amplifies the autoimmune reaction leading to disease manifestations. Genetic alterations in lineages other than B cells might explain other autoimmune syndromes where type I IFNs appear to be involved.
引用
收藏
页码:383 / 392
页数:10
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