Among the different phenotypic changes induced by contact sensitizers in dendritic cells and myeloid cell lines, CD86 appears to be a consensus marker, since constantly described as systematically up-regulated. To evaluate the robustness of this marker, interference of cytotoxicity on CD86 expression was investigated in U937 myelomonocytic cell line. In this study, cytotoxicity observed at 48 hr (reading-time for CD86 expression) after treatment with DNCB, NiSO(4) and pPD was shown to result from apoptosis taking place at earlier time points. This allergen-induced apoptosis was at least partly caspase-dependent as demonstrated by caspase-3 activation in response to DNCB and NiSO(4) and inhibition of DNCB-induced apoptosis by Z-VAD-fmk. Inhibition of apoptosis did not modify the stimulation index of CD86 expression in DNCB-treated cells, indicating that apoptosis did not interfere with up-regulation of CD86 expression. In addition, similar CD86 expression level was found in DNCB-treated cells whether calculated from the whole non-necrotic cell population including apoptotic cells or from viable non-apoptotic cell population only. Altogether, these results brought evidence that the presence of cells engaged in death process are not a confusing factor for CD86 expression in response to contact sensitizers. They also pointed out apoptosis as another possible key marker of cellular response to contact sensitizers.