Using polymerase chain reaction-restriction fragment length polymorphisms, we examined the NKG2DThr72Ala polymorphism in patients with cervical cancer (n=353) and controls (n=366) in a Polish population.
We demonstrate that NKG2D expressed on NKL cells is down-modulated by direct cell contact with cervical cancer cell lines HeLa, SiHa, and C33A, but not with non-tumorigenic keratinocytes (HaCaT).
Although the data were limited regarding functional polymorphism, it is conceivable that polymorphism of MICA may contribute to different degree of immune activation caused by different NKG2D-binding affinity, acting as a susceptible factor for development of cervical cancer.