Autoimmunity through cytokine-induced dendritic cell activation

被引：253

作者：

Banchereau, J ^{[1
]}

Pascual, V ^{[1
]}

Palucka, AK ^{[1
]}

机构：

[1] Baylor Inst Immunol Res, Dallas, TX 75204 USA

来源：

IMMUNITY | 2004年 / 20卷 / 05期

关键词：

D O I：

10.1016/S1074-7613(04)00108-6

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

We propose a model where autoimmunity can be viewed as a dynamic system driven by opposite vectors IFN-alpha/beta and TNF. These cytokines drive differentiation of distinct types of DCs, TNF-DCs, or lFN-DCs, which present different antigens leading to distinct autoimmune responses. When balanced, both cytokines synergize in protective immunity. When one of the cytokines prevails, autoimmunity occurs, Type I interferons (IFN-alpha/beta) playing a major role in systemic lupus erythematosus (SLE) and TNF playing a major role in rheumatoid arthritis. This model complements the Type 1/Type 2 paradigm. Therefore, immunity can be viewed as a dynamic system driven by two sets of opposite vectors: IFN-alpha/beta/TNF and IFN-gamma/IL-4.

引用

收藏

页码：539 / 550

页数：12

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