Comprehensive analysis of tumor necrosis factor-α-inducible protein 8-like 2 (TIPE2): A potential novel pan-cancer immune checkpoint
Related Experiment Video
Updated: Aug 26, 2025

Multiplexed Immunofluorescence Analysis and Quantification of Intratumoral PD-1+ Tim-3+ CD8+ T Cells
Published on: February 8, 2018
Kun-Hao Bai1,2, Yi-Yang Zhang1,2, Xue-Ping Li1,3
1State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, 651 Dongfeng East Road, Guangzhou 500020, Guangdong, China.
Abstract:
Tumor necrosis factor-α-inducible protein 8-like 2 (TIPE2) is encoded by TNFAIP8L2 and is a newly identified negative regulator of natural and acquired immunity that plays a critical function in maintaining immune homeostasis. Recently, CAR-NK immune cell therapy has been a focus of major research efforts as a novel cancer therapeutic strategy. TIPE2 is a potential checkpoint molecule for immune cell maturation and antitumor immunity that could be used as a novel NK cell-based immunotherapeutic approach. In this study, we explored the expression of TNFAIP8L2 across various tumor types and found that TNFAIP8L2 was highly expressed in most tumor types and correlated with prognosis. Survival analysis showed that TNFAIP8L2 expression was predictive of improved survival in cervical-squamous-cell-carcinoma (CESC), sarcoma (SARC) and skin-cutaneous-melanoma (SKCM). Conversely, TNFAIP8L2 expression predicted poorer survival in acute myeloid leukemia (LAML), lower-grade-glioma (LGG), kidney-renal-clear-cell-carcinoma (KIRC) and uveal-melanoma (UVM). Analysis of stemness features and immune cell infiltration indicated that TNFAIP8L2 was significantly associated with cancer stem cell index and increased macrophage and dendritic cell infiltration. Our data suggest that TNFAIP8L2 may be a novel immune checkpoint biomarker across different tumor types, particularly in LAML, LGG, KIRC and UVM, and may have further utility as a potential target for immunotherapy.
Insights
Tumor necrosis factor-α-inducible protein 8-like 2 (TIPE2) is a novel immune regulator. Its expression in tumors correlates with patient prognosis, suggesting TIPE2 as a potential biomarker and therapeutic target for cancer immunotherapy.
Area of Science:
- Immunology
- Oncology
- Molecular Biology
Background:
- Tumor necrosis factor-α-inducible protein 8-like 2 (TIPE2) is a key regulator of immune homeostasis.
- CAR-NK cell therapy is a promising cancer treatment strategy.
- TIPE2 may act as an immune checkpoint for NK cell-based immunotherapy.
Purpose of the Study:
- To investigate the expression of TNFAIP8L2 in various cancer types.
- To determine the prognostic value of TNFAIP8L2 expression.
- To explore the association of TNFAIP8L2 with cancer stemness and immune infiltration.
Main Methods:
- Analysis of TNFAIP8L2 expression data across multiple tumor types.
- Survival analysis to correlate TNFAIP8L2 expression with patient outcomes.
- Assessment of stemness features and immune cell infiltration in relation to TNFAIP8L2 levels.
Main Results:
- TNFAIP8L2 is highly expressed in most tumors and correlates with prognosis.
- Positive survival prediction for TNFAIP8L2 in CESC, SARC, and SKCM.
- Negative survival prediction for TNFAIP8L2 in LAML, LGG, KIRC, and UVM.
- TNFAIP8L2 is linked to cancer stem cell index and increased macrophage/dendritic cell infiltration.
Conclusions:
- TNFAIP8L2 is a potential immune checkpoint biomarker in various cancers, especially LAML, LGG, KIRC, and UVM.
- TNFAIP8L2 may serve as a target for novel immunotherapeutic strategies.
- Further research into TIPE2's role in immunotherapy is warranted.
More Related Videos
Related Concept Videos
Tumor Immunotherapy
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...

