Altered expression of CD226 and CD96 on natural killer cells in patients with pancreatic cancer.
The progression of pancreatic cancer (PC) is significantly associated with tumor immune escape, which may be associated with nature killer (NK) cell dysfunction. CD226, CD96, and TIGIT, which share the ligand CD155, play important roles in the regulation of NK cell function. The present study was conducted to investigate the roles of these molecules in NK cells from PC patients. Expression of these molecules on NK cells was detected from samples of 92 pancreatic cancer patients and 40 healthy controls. The expression of CD155 was also evaluated by immunohistochemistry in 88 pancreatic cancer tissues. The percentage of CD226+ and CD96+ NK cells was significantly lower in PC patients than in the healthy controls; however, the mean fluorescence intensity of CD226 and CD96 was not significantly different between the two groups. TIGIT expression on NK cells from PC patients was similar to that in the healthy controls. Additionally, the expression of CD226 was positively correlated with CD96. Further analysis demonstrated that the decrease in the percentage of CD226+ and CD96+ NK cells was associated with tumor histological grade and lymph node metastasis. Moreover, the CD155 levels in PC tissues were significantly higher than those in adjacent tissues. Our results suggest that a lower percentage of CD226+ and CD96+ NK cells may contribute to tumor immune escape in PC patients; moreover, the use of NK cells with high CD226 and CD96 expression to treat PC cells with high CD155 expression may have potential and should be explored in the future.
Department of General Surgery, Pancreas Centre, First Affiliated Hospital, Nanjing Medical University, Nanjing, P.R.China.
Yun-Peng
YP
Peng
Department of General Surgery, Pancreas Centre, First Affiliated Hospital, Nanjing Medical University, Nanjing, P.R.China.
Chun-Hua
CH
Xi
Department of General Surgery, Pancreas Centre, First Affiliated Hospital, Nanjing Medical University, Nanjing, P.R.China.|Institute of Tumor Biology, Jiangsu Province Academy of Clinical Medicine, Nanjing, P.R.China.
Yi
Y
Zhu
Department of General Surgery, Pancreas Centre, First Affiliated Hospital, Nanjing Medical University, Nanjing, P.R.China.
Ling-Di
LD
Yin
Department of General Surgery, Pancreas Centre, First Affiliated Hospital, Nanjing Medical University, Nanjing, P.R.China.
Ji-Shu
JS
Wei
Department of General Surgery, Pancreas Centre, First Affiliated Hospital, Nanjing Medical University, Nanjing, P.R.China.|Institute of Tumor Biology, Jiangsu Province Academy of Clinical Medicine, Nanjing, P.R.China.
Jing-Jing
JJ
Zhang
Department of General Surgery, Pancreas Centre, First Affiliated Hospital, Nanjing Medical University, Nanjing, P.R.China.
Xin-Chun
XC
Liu
Department of General Surgery, Pancreas Centre, First Affiliated Hospital, Nanjing Medical University, Nanjing, P.R.China.
Song
S
Guo
Department of General Surgery, Pancreas Centre, First Affiliated Hospital, Nanjing Medical University, Nanjing, P.R.China.
Yue
Y
Fu
Department of General Surgery, Pancreas Centre, First Affiliated Hospital, Nanjing Medical University, Nanjing, P.R.China.|Institute of Tumor Biology, Jiangsu Province Academy of Clinical Medicine, Nanjing, P.R.China.
Yi
Y
Miao
D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000096:biosynthesis* / Q000276:immunology; D000945:Antigens, Differentiation, T-Lymphocyte / Q000096:biosynthesis* / Q000276:immunology; D005260:Female; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010190:Pancreatic Neoplasms / Q000276:immunology* / Q000378:metabolism; D019139:Tumor Escape / Q000276:immunology*; D000098862:T Lineage-Specific Activation Antigen 1
D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D000098862:T Lineage-Specific Activation Antigen 1; C116131:CD96 antigen
CD226; CD96; NK cells; TIGIT; pancreatic cancer