CD226, TIGIT and CD96 regulate NK cell function and participate in anti-tumor immunity.
- Author:
Huiyuan ZHANG
1
,
2
;
Ruiyan LIU
3
;
Yusi ZHANG
4
;
Xiaobin LIU
5
;
Lihua CHEN
6
Author Information
1. Medical School of Yan'an University, Yan'an 716000
2. Department of Immunology, Basic Medical Science Academy, Air Force Medical University, Xi'an 710032, China.
3. Cadet Regiment, Basic Medical Science Academy, Air Force Medical University, Xi'an 710032, China.
4. Department of Immunology, Basic Medical Science Academy, Air Force Medical University, Xi'an 710032, China.
5. Medical School of Yan'an University, Yan'an 716000, China. *Corresponding author, E-mail: lxb2411817@163.com.
6. Department of Immunology, Basic Medical Science Academy, Air Force Medical University, Xi'an 710032, China. *Corresponding author, E-mail: chenlh@fmmu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Ligands;
Receptors, Immunologic;
Receptors, Natural Killer Cell;
Killer Cells, Natural;
Antigens, CD
- From:
Chinese Journal of Cellular and Molecular Immunology
2023;39(9):852-856
- CountryChina
- Language:Chinese
-
Abstract:
CD226 is an activated receptor on the surface of natural killer (NK) cells. It competes with TIGIT and CD96 to bind to ligands such as CD155 on the surface of tumor cells and mediates the killing function of NK cells. Although TIGIT and CD96 have other binding ligands in the tumor microenvironment, they compete to bind CD115 ligands with higher affinity and inhibit the activity of NK cells, which allows tumor cells to evade killing. Therefore, studying the expression patterns of these three NK cell surface receptors in different tumors and monitoring their binding ability with ligands will help us to explore new tumor treatment strategies. This article reviews the role and mechanism of CD226, TIGIT, CD96 and other NK cell receptor molecules in regulating NK cell function in anti-tumor immune response.
