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In the CD56bright NK-cell subset, cells expressing NKp46 and DNAM-1 �C both of which stimulate NK-cell functions �C were significantly less abundant in patients Rapamycin (p this website CD107a is transferred from cytolytic granules onto the cell surface, surface CD107a labeling can therefore be used as a surrogate marker for cytotoxic activity . We assessed CD107a labeling on NK cells from 11 patients and 15 HCs, NK cells from patients AP24534 in vitro had a strongly reduced capacity to delocalize CD107a after stimulation both with K562 (median experimental/control ratios: 2.0 for patients versus 4.4 for HCs; p = 0.0003) and with rituximab + Raji (median experimental/control ratios: 2.5 for patients versus 6.3 for HCs; p = 0.0005; Fig.?2A). Stimulating DLBCL NK cells with IL-2 during cytotoxicity assays increased their ADCC capacity slightly (median of experimental/control ratios: 1.7 in medium versus 2.4 with IL-2; p = 0.043) but did not fully restore ADCC to the levels measured for HCs (Fig.?2B). The CD107a experimental/control ratio in patients was also found to positively correlate with CD16 expression after stimulation by rituximab + Raji (Rho = 0.7; p = 0.020; Fig.?2C), but not after exposure to K562 (Rho = 0.2; p = 0.509). In our cohort, CD16 expression levels did not significantly associate with FCGR3A polymorphism (data not shown). Adding IL-2 to culture medium increased CD16 expression on NK cells from HCs, but this effect was very weak or negligible on DLBCL NK cells (data not shown). Taken together, these results confirmed that the reduced CD16 expression on patients�� NK cells was, at least partially, responsible for the impaired rituximab-mediated ADCC measured.