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Study of Natural Killer Cell Stimulatory Receptor NKG2D and its Ligand MICA in Patients with Cervical Cancer / 医学研究杂志
Article in Zh | WPRIM | ID: wpr-565768
Responsible library: WPRO
ABSTRACT
Objective To investigate the expression of NKG2D in peripheral blood of patients with cervical cancer,CIN,hysteromyoma and health person,and the expression of the human MHC class I chain-related gene A(MICA)on the correspondent tumor tissues.To discuss the anti-cervical cancer mechanism of NKG2D-MICA and immune escaping of cancer.Methods Flow cytometry analysis was used to detect the expression of NKG2D in the peripheral blood of patients with cervical cancer,CIN,hysteromyoma and health person.The expressions of MICA in part of the correspondent tissues were examined by means of reverse transcription-polymerase chain relation(RT-PCR).Results The expression of NKG2D in the patients with cervical cancer,CIN,hysteromyoma and health person were(76.87?9.39)%、(81.84?7.94)%、(86.77?8.68)%、(93.968?4.9)%,respectively.Compared with the normal group,the NKG2D expression in the particular disease group was of statistical significance,however,it is not statistically significant in the comparison in the particular disease group.The rate of MICA mRNA expression in cervical cancer was significantly higher than that in hysteromyoma and health tissues,and its difference is of statistical significance.But it is not statistically significant for the normal group to compare with the other group.Conclusion The activity of NK cell and the anti-cancer cellular immunity level reduce in patients with cervical cancer.The decrease of the receptor NKG2D is a reason for the descend of the activity of NK cells.MICA mRNA expression increases in the cervical cancer,and it has the tendency of up-regulation with the progress of pathological changes.It is relative to malignant transformation from cervical squamous intraepithelial lesion to cervical cancer;the immune-escape of cervical cancer probably is relative to the down-regulation of NKG2D and the up-regulation of its ligand MICA.
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Full text: 1 Index: WPRIM Language: Zh Journal: Journal of Medical Research Year: 2006 Type: Article
Full text: 1 Index: WPRIM Language: Zh Journal: Journal of Medical Research Year: 2006 Type: Article