Analysis of the Expression of Surface Receptors on NK Cells and NKG2D on Immunocytes in Peripheral Blood of Patients with Nasopharyngeal Carcinoma

Document Type : Research Articles


1 Department of Radiation Oncology, Fujian Cancer Hospital, Fujian Medical University Cancer Hospita, Fuzhou, Fujian, China

2 Provincial Clinical MedicineFujian Medical University Cancer Hospita, Fuzhou, Fujian, China.

3 Fujian Provincial Key Laboratory of Translational Cancer Medicine, Fujian Medical University Cancer Hospita, Fuzhou, Fujian, China.

4 Laboratory of Immuno-Oncology, Fujian Cancer Hospital, Fujian Medical University Cancer Hospita, Fuzhou, Fujian, China.

5 Department of Radiotherapy, First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian,China.

6 State Key Laboratory for Emerging Infectious Diseases, Department of Microbiology and the Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The University of Hong Kong, Hong Kong SAR, China.


Background: The aberrant expression of surface receptors on immunocytes may represent potential markers of tumor
escape for nasopharyngeal carcinoma (NPC). The aim of this study was to investigate the expression of representative
receptors on natural killer (NK) cells and NK group 2, member D (NKG2D) on immunocytes in the peripheral blood
of patients with NPC. Methods: Patients (n = 64) with NPC prior to initiation of treatment were defined as the study
group. Healthy volunteers (n = 31) served as the control group. The expression of NK cells and NKT cells; the triggering
receptors NKp30, NKp44, and NKp46 on NK cells; the activating receptor NKG2D on NK cells, CD4+ T cells, and
CD8+ T cells; and the inhibitory receptors CD158b and CD159a on NK cells were analyzed by flow cytometry in the
two groups. Results: Here, our study showed that no differences were observed in terms of the numbers of NK cells or
NKT cells, or the expression of CD158b and CD159a on the surface of NK cells between the two groups. Nevertheless,
the expression levels of NKp30 and NKp46 on NK cells in the NPC patients were significantly lower than in the healthy
individuals (P < 0.05). No differences existed in the expression of NKG2D on NK cells, but NKG2D on CD8+ T cells
showed a markedly lower expression in the study group (P < 0.001). Conclusions: Our findings may reflect a possible
mechanism of immune evasion for NPC. The enhancement of immunotherapy concerning NKp30, NKp46, and NKG2D
may be an innovative treatment strategy for patients with NPC.


Main Subjects