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Allogeneic stem cell transplantation (allo-SCT) with or without donor lymphocyte infusions (DLI) is the only curative option for several hematological malignancies. Unfortunately, allo-SCT is often associated with GvHD, and patients often relapse. We therefore aim to improve the graft-versus-tumor effect, without increasing the risk of GvHD, by targeting hematopoietic lineage-restricted and tumor-associated minor histocompatibility antigens using peptide-loaded dendritic cell (DC) vaccinations. In the present multicenter study, we report the feasibility, safety and efficacy of this concept. We treated nine multiple myeloma patients with persistent or relapsed disease after allo-SCT and a previous DLI, with donor monocyte-derived mHag-peptide-loaded DC vaccinations combined with a second DLI. Vaccinations were well tolerated and no occurrence of GvHD was observed. In five out of nine patients, we were able to show the induction of mHag-specific CD8+T cells in peripheral blood. Five out of nine patients, of which four developed mHag-specific T cells, showed stable disease (SD) for 3.5–10 months. This study shows that mHag-based donor monocyte-derived DC vaccination combined with DLI is safe, feasible and capable of inducing objective mHag-specific T-cell responses. Future research should focus on further improvement of the vaccination strategy, toward translating the observed T-cell responses into robust clinical responses.

Administation of neutralizing anti‐TNFα antibodies did not prevent Plasmodium bergheiinduced cerebral malaria (CM) in C57Bl/6 mice, when given at different dosages and time intervals. Elevated concentrations of immunoreactive TNFα were found in the circulation but no bioactive TNFα could be detected in mice developing CM. Furthermore, elevated TNFα receptor concentrations were measured in the plasma of mice developing CM. Plasma of these mice neutralized bioactive recombinant‐mouse TNFα indicating that a part of the plasma TNFα‐receptors were not complexed with TNFα. The apparent absence of free TNFα probably explains why treatment with antibodies against TNFα failed to prevent development of CM.