Abstract
Abstract Natural killer (NK) cells belong to the innate immune system and are able to control various microbial infections as well as tumor cell burden. NK cells can be divided into two different subsets based on the expression of the two surface markers: CD16 and CD56. Two major NK cell populations are present in the blood; one that express high levels of CD56 and low levels of CD16; named CD56Bright cells and a bigger population (90%) that express CD56 in inermediate levels and express high levels of CD16, named CD56Dim. The latter poultion is more mature and more cytotoxic, while the CD56Bright cells produce high levels of cytokines. The human Cytomegalovirus (HCMV) is a β herpesvirus with a double-stranded DNA genome which encodes a broad range of genes that involved in immune evasion and regulation. Among these, are 3 viral chemokines named vCXCL1, vCXCL2 and UL128. The function of these 3 viral chemokines is not completely understood. Using fusion and recombinant viral proteins we showed that all three chemokines are capable of binding to the CD56Dim CD16Pos NK cell population. We demonstrate that only one of them, the vCXCL1, can surprisingly cause NK cells migration and we identified the chemokine receptors involved in these migrations.
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