Augmented serum level of major histocompatibility complex class I-related chain A (MICA) protein and reduced NKG2D expression on NK and T cells in patients with cervical cancer and precursor lesions

Peripheral blood with or without heparin was collected to obtain mononuclear cells or sera, respectively. Serum sMICA levels were measured by ELISA and NKG2D-expressing immune cells were analyzed by flow cytometry. Also, a correlation analysis was performed to associate sMICA levels with either NKG2D expression or with the stage of the lesion.Significant amounts of sMICA were detected in sera from nearly all patients. We found a decrease in the number of NKG2D-expressing NK and T cells in both cervical cancer and lesion groups when compared to healthy donors. Pearson analysis showed a negative correlation between sMICA and NKG2D-expressing T cells; however, we did not find a significant correlation when the analysis was applied to sMICA and NKG2D expression on NK cells.Our results show for the first time that high sMICA levels are found in sera from patients with both cervical cancer and precursor lesions when compared with healthy donors. We also observed a diminution in the number of NKG2D-expressing NK and T cells in the patient samples; however, a significant negative correlation between sMICA and NKG2D expression was only seen in T cells.Cervical cancer is the second most common malignant tumor in women worldwide, and the most common tumor in developing countries including Mexico, the site of this study [1-3]. Infection with high-risk human papilloma virus (HPV) is considered the major etiological factor of HPV-related premalignant lesions and cervical cancer [4-7]. Virtually all cervical carcinoma patients (99.7%) have shown to be HPV-DNA carriers [8]. Although HPV prevalence is very common in sexually active women [9], the infection in the majority of cases is transient, clearing in a short period of time without progression to clinical lesions [10-12]. In a minority of cases, HPV presence is established as a persistent infection. It is thought that viral persistence leads to progression from low-grade squamous intraepithelial lesions (LSIL) to high-grade squ