期刊
SEMINARS IN IMMUNOLOGY
卷 31, 期 -, 页码 64-75出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.smim.2017.07.011
关键词
Natural killer cells; Checkpoint; PD-1; CTLA-4; Immunotherapy; BiKE; TriKE
类别
资金
- NIH [P01 CA111412, P01 CA65493, R35 CA197292, T32 HL007062]
- U.S. Department of Defense [CA150085]
- NATIONAL CANCER INSTITUTE [R21CA150085, P01CA065493, P30CA077598, P01CA111412, R35CA197292] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [T32HL007062] Funding Source: NIH RePORTER
Natural killer (NK) cells have long been known to mediate anti-tumor responses without prior sensitization or recognition of specific tumor antigens. However, the tumor microenvironment can suppress NK cell function resulting in tumor escape and disease progression. Despite recent advances in cytokine therapy and NK cell adoptive transfer, tumor expression of ligands to NK expressed checkpoint receptors can still suppress NK mediated tumor lysis. This review will explore many of the checkpoint receptors tumors utilize to manipulate the NK cell response as well as some of the current and upcoming pharmacological solutions to limit tumor suppression of NK cell function. Furthermore, we will discuss the potential to use these drugs in combinational therapies with novel antibody reagents such as bi- and tri-specific killer engagers (BiKEs and TriKEs) against tumor-specific antigens to enhance NK cell-mediated tumor rejection.
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