期刊
CANCERS
卷 13, 期 4, 页码 -出版社
MDPI
DOI: 10.3390/cancers13040596
关键词
CD4+T cells; tumor; immunotherapy
类别
资金
- Deutsche Forschungsgemeinschaft, Collaborative Research Center 1399 [SFB 1399]
- Deutsche Forschungsgemeinschaft under Germany's Excellence Strategy [EXC 2180-390900677]
- University of Tubingen
CD4+ T cells, bearing the CD4 co-receptor, are a heterogeneous group of T lymphocytes that play a crucial role in the antitumor immune response by directly or indirectly killing tumor cells. Research is increasingly focusing on both CD4+ and CD8+ T cell subsets in cancer immunotherapy approaches.
Simple Summary T cells bearing the co-receptor CD4 on their cell surface are a heterogeneous group of T lymphocytes that exert pro- or anti-inflammatory functions. Evidence from mouse models and cancer patients reveal that various CD4+ T cell subsets play an antagonistic role in the antitumor immune response. This review summarizes current knowledge on CD4+ T cell subsets, on how they impact tumor growth in patients, and which role these cells play in newest cancer immunotherapies. Cancer immunotherapy activates the immune system to specifically target malignant cells. Research has often focused on CD8+ cytotoxic T cells, as those have the capacity to eliminate tumor cells after specific recognition upon TCR-MHC class I interaction. However, CD4+ T cells have gained attention in the field, as they are not only essential to promote help to CD8+ T cells, but are also able to kill tumor cells directly (via MHC-class II dependent recognition) or indirectly (e.g., via the activation of other immune cells like macrophages). Therefore, immunotherapy approaches have shifted from only stimulating CD8+ T cells to targeting and assessing both, CD4+ and CD8+ T cell subsets. Here, we discuss the various subsets of CD4+ T cells, their plasticity and functionality, their relevance in the antitumor immune response in patients affected by cancer, and their ever-growing role in therapeutic approaches for human cancer.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据