Paradoxical effects of targeting TNF signalling in the treatment of autoimmunity

被引：0

作者：

Xin Chen

Joost J. Oppenheim

机构：

[1] State Key Laboratory of Quality Research in Chinese Medicine,

[2] Institute of Chinese Medical Sciences,undefined

[3] University of Macau,undefined

[4] Macao SAR 999078,undefined

[5] China; and the Cancer and Inflammation Program,undefined

[6] Center for Cancer Research,undefined

[7] National Cancer Institute,undefined

[8] Frederick,undefined

[9] Maryland 21702,undefined

[10] USA.,undefined

[11] and the Cancer and Inflammation Program,undefined

[12] Center for Cancer Research,undefined

[13] National Cancer Institute,undefined

[14] Frederick,undefined

[15] Maryland 21702,undefined

[16] USA.,undefined

[17] Cancer and Inflammation Program,undefined

[18] Center for Cancer Research,undefined

[19] National Cancer Institute,undefined

来源：

Nature Reviews Rheumatology | 2016年 / 12卷

关键词：

D O I：

暂无

中图分类号：

学科分类号：

摘要：

Adalimumab, an anti-TNF monoclonal antibody used to treat rheumatoid arthritis and other autoimmune disorders, paradoxically enhances the capacity of TNF to expand TNF receptor type II-expressing regulatory T cells. This provocative finding opens a new avenue for exploring the mechanisms that underlie efficacy, non-responsiveness and adverse effects associated with therapeutic targeting of TNF signalling.

引用

页码：625 / 626

页数：1

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