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TWEAK as a target for therapy in systemic lupus erythematosus

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Abstract

Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a recently identified proinflammatory cytokine of the TNF superfamily. Through activation of the fibroblast growth factor-inducible 14 (Fn14) receptor, TWEAK regulates cell proliferation, cell death and inflammation. The available evidences have indicated that TWEAK might be a target for therapeutic intervention in renal, vascular injury and neuropathy. Since renal, vascular and neuropsychiatric complications are frequently encountered in systemic lupus erythematosus (SLE)—a systemic autoimmune disease, TWEAK-Fn14 pathway may be implicated in the pathogenesis of SLE. In this review, we will discuss the TWEAK-Fn14 pathway and the therapeutic potential of modulating this pathway in SLE.

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Acknowledgments

This work was supported by grants from the key program of National Natural Science Foundation of China (30830089) and the Specialized Research Fund for the Doctoral Program of Higher Education of China (20070366002).

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The authors declared no competing interests.

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Correspondence to Dong-Qing Ye.

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Rui-Xue Leng and Hai-Feng Pan are contributed equally to this work and should be considered co-first authors.

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Leng, RX., Pan, HF., Qin, WZ. et al. TWEAK as a target for therapy in systemic lupus erythematosus. Mol Biol Rep 38, 587–592 (2011). https://doi.org/10.1007/s11033-010-0144-9

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  • DOI: https://doi.org/10.1007/s11033-010-0144-9

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