We knew from previous experiments that PBMCs from healthy donors, which were incubated with gp350+ exosomes, efficiently re-stimulated an autologous gp350-specific CD4+ T-cell clone (data not shown). These experiments implicated that gp350, which is equally transferred to B-CLL cells by CD154+/gp350+ exosomes, can act as a neo-antigen in B-CLL cells, which are normally not infected with EBV [18] . This is a very interesting aspect because B-CLL patients usually maintain a robust and easily recruited CMV- [19] and EBV-specific T-cell response [2] although their T cells in general are functionally impaired. For instance, B-CLL cells infected with EBV or loaded with CMVpeptides are efficiently killed by autologous T lymphocytes from B-CLL patients [18, 20] . We thus aimed at investigating whether gp350 serves as a viral neo-antigen in exosome-treated leukemic cells and whether these cells become targets for gp350-specific autologous T lymphocytes. We stimulated PBMCs from B-CLL patients three times with CD154+/gp350+ exosomes as described above and elucidated the specificities and cytolytic potential of the activated T cells. To this end, we incubated autologous PBMCs for 24 hours with either CD154+/gp350+ exosomes, CD154+/gp350-exosomes or unmodified 293 exosomes or left them untreated. The next day, these cells were labeled with calcein and used as targets for autologous effector T cells. As shown in Figure 3 , T cells generated by stimulation with gp350+/ CD154+ exosomes efficiently killed autologous PBMCs that had been activated with CD154+/gp350-or CD154+/gp350+ exosomes as quantified by the release of calcein. Of interest, we did not observe notable activation of T cells against 293 proteins as PBMCs incubated with exosomes from non-transfected 293 cells were lysed to almost the same extent as non-activated autologous PBMCs.