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CD155 and its receptors in cancer immune escape and immunotherapy
Ruijia Zhou1, Shiyin Chen1, Qiwen Wu1
1NHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Translational Radiation Oncology, Hunan Cancer Hospital and The Affiliated Cancer Hospital, Xiangya School of Medicine, Central South University, Changsha, Hunan, China; Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China; Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Disease Genome Research Center, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Abstract:
In recent years, there have been multiple breakthroughs in cancer immunotherapy, with immune checkpoint inhibitors becoming the most promising treatment strategy. However, available drugs are not always effective. As an emerging immune checkpoint molecule, CD155 has become an important target for immunotherapy. This review describes the structure and function of CD155, its receptors TIGIT, CD96, and CD226, and summarizes that CD155 expressed by tumor cells can upregulate its expression through the DNA damage response pathway and Ras-Raf-MEK-ERK signaling pathway. This review also elaborates the mechanism of immune escape after binding CD155 to its receptors TIGIT, CD96, and CD226, and summarizes the current progress of immunotherapy research regarding CD155 and its receptors. Besides, it also discusses the future direction of checkpoint immunotherapy.
Insights
CD155 is an emerging target in cancer immunotherapy. This review details CD155
Area of Science:
- Immunology
- Oncology
- Molecular Biology
Background:
- Cancer immunotherapy has seen significant advancements, particularly with immune checkpoint inhibitors.
- However, the efficacy of current treatments remains limited for many patients.
- CD155 has emerged as a crucial immune checkpoint molecule with therapeutic potential.
Purpose of the Study:
- To review the structure and function of CD155 and its receptors (TIGIT, CD96, CD226).
- To summarize the mechanisms by which tumor cells upregulate CD155 expression.
- To elaborate on immune escape mechanisms mediated by CD155-receptor interactions and discuss future immunotherapy directions.
Main Methods:
- Literature review and synthesis of existing research on CD155 and its role in cancer immunology.
- Analysis of molecular pathways involved in CD155 expression and regulation.
- Examination of preclinical and clinical data on CD155-targeted immunotherapies.
Main Results:
- CD155 expression on tumor cells is upregulated via DNA damage response and Ras-Raf-MEK-ERK pathways.
- Binding of CD155 to its receptors TIGIT, CD96, and CD226 facilitates tumor immune escape.
- Current research highlights CD155 and its receptors as promising targets for novel cancer immunotherapies.
Conclusions:
- CD155 plays a critical role in tumor immune evasion, making it a key target for enhancing cancer immunotherapy.
- Understanding the regulatory pathways and receptor interactions of CD155 is vital for developing effective therapeutic strategies.
- Further research into CD155-targeted therapies holds significant promise for improving patient outcomes in cancer treatment.
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