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Int J Biol Sci 2018; 14(4):398-405. doi:10.7150/ijbs.23268


Tumor Necrosis Factor-α Induced Protein 8: Pathophysiology, Clinical Significance, and Regulatory Mechanism

Lei Zhang1,2, Ran Liu3, Ying-yi Luan1, Yong-ming Yao1✉

1. Trauma Research Center, First Hospital Affiliated to the Chinese PLA General Hospital, Beijing 100048, People's Republic of China.
2. Emergency Department, The General Hospital of the Chinese PLA Rocket Force, Beijing 100088, People's Republic of China.
3. Department of Endocrinology, 307th Hospital of the Chinese PLA, Beijing 100071, People's Republic of China.


Tumor necrosis factor-α-induced protein-8 (TNFAIP8) is the earliest discovered component of TNFAIP8 family [tumor necrosis factor-α-induced protein-8 like (TIPE) family]. TNFAIP8 contains a putative death effector domain (DED) homologous to DED II in FLIP (Fas-associated death domain-like interleukin-1β-converting enzyme-inhibitory protein), which may affect cell survival/death process. Recently, it has been demonstrated that TNFAIP8 could inhibit apoptosis and autophagy in various types of cells. Moreover, TNFAIP8 level fluctuated evidently in patients with inflammatory, malignant, and autoimmune diseases, indicating that it might be an anti-apoptotic and oncogenetic protein. Herein we will review the discovery, gene/protein structure, pathophysiological functions, and clinical significance of TNFAIP8 together with its potential regulatory mechanism.

Keywords: Tumor Necrosis Factor-α Induced Protein-8, Inflammation, Tumor, Apoptosis, Autophagy, Immune Response

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license ( See for full terms and conditions.
How to cite this article:
Zhang L, Liu R, Luan Yy, Yao Ym. Tumor Necrosis Factor-α Induced Protein 8: Pathophysiology, Clinical Significance, and Regulatory Mechanism. Int J Biol Sci 2018; 14(4):398-405. doi:10.7150/ijbs.23268. Available from