Detection of the NK cell stimulatory receptor NKG2D and its soluble ligand MICA in patients with esophageal carcinoma
10.3760/cma.j.issn.1006-9801.2009.05.007
- VernacularTitle:食管癌患者自然杀伤细胞活化性受体NKG2D及其分泌性配体sMICA的检测
- Author:
Jianping YAN
;
Yujie ZHANG
;
Shiping GUO
;
Lijuan QIAO
- Publication Type:Journal Article
- Keywords:
Esophageal neoplasms;
Killer cells,natural;
Receptors,neurokinin-2;
Genes,MHCclass Ⅰ
- From:
Cancer Research and Clinic
2009;21(5):308-310
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression of NKG2D peripheral blood of patients with esophageal carcinoma and expression of the soluble form of major histocompatibility complex class Ⅰ-related chain A (MICA). To analyze and discuss the function of NKG2D in anti-esophageal carcinoma mechanism and its relation with escape of immunosurveillance of cancer. Methods Flow cytometry analysis was used to detect NKG2D in the peripheral blood of 50 patients with esophageal carcinoma and 25 normal control individuals. Enzyme-linked immunoabsorbent assay was used to measure serum levels of soluble MICA. Results The expression of NKG2D were(87.25±3.06), (88.38±4.24), (92.46±1.46) respectively. Compared with the normal control individual, the expression of NKG2D in esophageal carcinoma group was significantly low; Among patients categorized according to most disease parameters tested (tumor size, grade of differentiation, regional lymph node status, disease stage), soluble MICA levels in sera did not statistically differ from those in normal control individuals. Patients with stage Ⅳ disease and/or regional lymph node metastasis, exhibited significantly higher serum levels of soluble MICA than control individuals. Conclusion The activity of NK cell and the anti-cancer cellular immunity level reduce in patients with esophageal carcinoma. The decrease of the receptor NKG2D is a reason for the descend of the the activity of NK cells. The escape of immunosurveiilance with esophagal carcinoma may correlate with down-regulate of NKG2D expression and up-regulate of sMICA.
