AuthOr’s VIew AuthOr’s VIew

In the human hematopoietic system, CD56 is considered as a classical surface marker of natural killer (NK) cells and it is used to identify the two main NK-cell subsets: CD56bright and CD56dim. Despite its stringent association with NK cells, the expression of CD56 has also been detected on other human lymphoid cells includ-ing NKT cells and activated T cells.1 Common to all these CD56-expressing cell types is a cytotoxic function, strongly suggesting that the expression of CD56 in the hematopoietic system is restricted to cytotoxic effector cells. In two recent papers, we have shown that human plasmacytoid and myeloid dendritic cells (DCs) can also adopt a CD56+ phenotype and acquire cytotoxic functions. In the first study,1 we revealed that the activation of plasmacytoid DCs (pDCs) with the tick-borne encephalitis vaccine FSME, which presumably acts as a Toll-like receptor (TLR) ligand, causes a partial upregulation of CD56 on their cell surface. Despite the expression of CD56, FSME-activated pDCs fulfilled all phe-notypic and functional characteristics to be classified as DCs, including a potent allostimulatory ability and the capac-ity to prime naive antigen-specific T-cell responses. Intriguingly, in addition to these CD56 marks human dendritic cell subsets with cytotoxic potential Dessie roothans,1 evelien smits,1,2 eva Lion,1 Jurjen tel3, † and sébastien Anguille1,2,†,* 1Vaccine and Infectious Disease Institute (VAXINFeCtIO); Laboratory of experimental hematology; university of Antwerp; Antwerp, Belgium