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MICB是NK细胞活化受体NKG2D的配基,可在应激作用下与NKG2D作用,在NK细胞对病毒感染细胞和肿瘤细胞的杀伤作用的有效发挥中具有重要的作用。以色列的一个研究小组在2007年7月的《science》上报道,在病毒感染过程中,人巨细胞病毒miRNA(hcmv-miR-UL112)可以特异地下调MICB的表达,导致其与NKG2D结合的下降,从而减弱了NK细胞的杀伤作用。该揭示了一种新的免疫逃避的机制,这种建立在miRNA基础上的机制被认为可能在人巨细胞病毒感染的过程中起作用。
MICB is the ligand of NKG2D, an NK cell activation receptor, which plays an important role in NKG2D under stress and plays an important role in the effective killing effect of NK cells on virus-infected cells and tumor cells. A team from Israel reported in the July 2007 issue of “science” that human cytomegalovirus miRNA (hcmv-miR-UL112) can specifically down-regulate the expression of MICB during virus infection, resulting in a decrease of its binding to NKG2D , Thus weakened the killing effect of NK cells. This reveals a novel mechanism of immune evasion, a mechanism based on miRNAs that is thought to play a role in human cytomegalovirus infection.