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Role of the TWEAK/Fn14 pathway in autoimmune diseases

Wang-Dong Xu1, Yi Zhao1, Yi Liu2

  • 1Department of Rheumatology and Immunology, West China Hospital, Sichuan University, 37 Guoxue Xiang, Chengdu, 610041, Sichuan, People's Republic of China.

Immunologic Research
|December 15, 2015
PubMed

TNF-like weak inducer of apoptosis (TWEAK) is a member of the TNFSF ligands, initially synthesized as a type II transmembrane protein. TWEAK signaling occurs via binding to Fn14, a type I transmembrane receptor belonging to the TNF receptor superfamily. TWEAK/Fn14 activation controls several cellular responses, including proliferation, angiogenesis, induction of inflammatory cytokines. Studies have indicated that expression of TWEAK/Fn14 was dysregulated in autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, inflammatory bowel disease. Functional analysis suggested that TWEAK/Fn14 may play an important role in the development of these diseases. In this review, we discuss the TWEAK/Fn14 pathway and its significant role in autoimmune disorders. The information obtained may lead to a better understanding of the insights into TWEAK/Fn14 in these autoimmune diseases.

Keywords:
AutoimmuneFn14TWEAK

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