// Jinhua Xie 1, * , Ji Wang 2, * , Shouliang Cheng 3 , Liangfeng Zheng 3 , Feiyue Ji 3 , Lin Yang 4 , Yan Zhang 1 , Haoming Ji 1 1 Cancer Center, Hai’an Hospital Affiliated to Nantong University, Hai’an, China 2 Department of Oncology, the Second Affiliated Hospital of Soochow University, Suzhou, China 3 The Central Laboratory, Hai’an Hospital Affiliated to Nantong University, Hai’an, China 4 Cyrus Tang Hematology Center, Soochow University, Suzhou, China * Co-first authors Correspondence to: Haoming Ji, email: jihaomingha@163.com Keywords: esophageal cancer, immune checkpoints, PD-1, TIM-3, cancer immunotherapy Received: June 29, 2016 Accepted: August 16, 2016 Published: August 25, 2016 ABSTRACT Inhibition of immune checkpoint proteins (checkpoints) has become a promising anti-esophageal cancer strategy. We here tested expressions of immune checkpoints in human esophageal cancers. Our results showed the expressions of many immune checkpoints, including CD28, CD27, CD137L, programmed death 1 (PD-1), T cell immunoglobulin mucin-3 (TIM-3), T cell Ig and ITIM domain (TIGIT), CD160, cytotoxic T lymphocyte antigen 4 (CTLA-4), CD200, CD137 and CD158, were dysregulated in peripheral T cells of esophageal cancer patients. Further, the expressions of PD-1, TIM-3 and TIGIT were upregulated in tumor infiltrating lymphocytes (TILs), which might be associated with TILs exhaustion. Meanwhile, the expressions of PD-1 and TIM-3 on CD4+ T cells were closely associated with clinic pathological features of esophageal cancer patients. These results indicate that co-inhibitory receptors PD-1, TIM-3 and TIGIT may be potential therapeutic oncotargets for esophageal cancer.
No takes yet. Share an insight, caveat, or question.
Xie et al. (2016) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: