RESUMEN
The killer cell immunoglobulin-like receptor (KIR) is located in 100-200kb region of the leukocyte receptor complex (LRC) on chromosome 19. KIR, mainly expresses on the surface of natural killer (NK) cells, is divided into inhibitory and activated receptor in function. Tumor cells could evade the killing of NK cells by regulating down the expression of HLA molecules on the cell surface. KIR molecules regulate the killing effect of NK cells by combining with human leukocyte antigen (HLA) to conduct inhibitory and active signals. In recent years, KIR and its immune regulation on tumors have become a research hotspot. The article reviews the research progress of KIR and its association with tumors, especially the correlation between KIR and high incidence of nasopharyngeal carcinoma (NPC) in Guangdong and Guangxi of China.
RESUMEN
Background and purpose:To date, it mainly depended on imaging examination for detection of residual lesions, recurrence and distant metastasis, evaluation the sensitivity of radiotherapy and chemotherapy, and prognosis in nasopharyngeal carcinoma (NPC). Thus, searching for new tumor markers for NPC early diagnosis and individualized treatment is still merited. This study was aimed to investigate the expressions of serum macrophage inflammatory protein (MIP)-3α and cystatin A in patients with NPC before and after treatment, and to explore two markers’ value in NPC diagnosis, clinicopathological characteristics and clinical outcome assessment. Methods:The serum levels of MIP-3αand cystatin A in 140 primary NPC patients without distant metastasis before and after treatment were detected by enzyme-linked immunosorbent assay (ELISA) and compared with those in 100 healthy controls. Results:The sensitivity of MIP-3αand cystatin A were 92.1%and 42.1%, respectively;and the specificity of MIP-3αand cystatin A were 86.0%and 85.0%, respectively. All 140 NPC patients had complete remission (CR) or partial remission (PR). Serum levels of MIP-3αand cystatin A in pre-treatment patients with NPC were higher than those in post-treatment patients and controls. Serum MIP-3αand cystatin A levels were associated with overall stage of NPC, and MIP-3αwas also associated with T classification of NPC. The serum MIP-3αlevel in NPC with CR after treatment reduced to the level in control group, and that was still significantly higher in NPC with PR than in control group. No significant difference was found in the serum cystatin A level between NPC with CR or PR after treatment and control group. During 1-year follow-up, the post-treatment serum levels of MIP-3αand cystatin A were significantly higher in patients with distant metastasis than in patients without distant metastasis and controls. There was found statistically significant correlation between MIP-3α and cystatin A.Conclusion:MIP-3α may be a potential marker of NPC serological diagnosis. The detection of serum MIP-3αand cystatin A may contribute to the NPC staging and prediction of short-term clinical outcomes.