LAUSR

Although multiple myeloma (MM) has become more treatable in the past decade by application of proteasome inhibitors (PI) and immunomodulatory drugs (IMiDs) [1], there is an urgent need for development of novel treatment alternatives. Monoclonal antibodies (mAbs) have become of growing interest as promising approaches over the last few years. Since rituximab, an anti-CD20 mAbs, is efficiently established in the treatment of B-cell NHL, previous attempts for application of this mAbs in MM patients have been rather unsuccessful [2]. However, several potential surface targets for therapeutic antibodies have been evaluated. Especially the type II single-chain transmembrane glycoprotein CD38, which is highly expressed on multiple myeloma cells, seems to be a promising candidate for immunotherapy of MM. The human monoclonal antibody MOR202 directed against CD38 undergoes currently clinical trials for treatment of relapsed or refractory MM [3]. Although anti-CD38 antibodies have shown substantial activity as monotherapy, observations from preclinical studies and recent clinical trials indicate that combination with IMiDs such as lenalidomide further enhances their anti-MM efficacy [4]. Macrophages mediate antibody-dependent cellular phagocytosis (ADCP) and antibody-dependent cellmediated cytotoxicity (ADCC) but also serve in a MM-supportive role as so-called myeloma-associated macrophages (MAMs) [5]. Despite their clear abundance in close proximity to MM-cells, little is known of their potential role in mediating the therapeutic antibody effects and whether or how lenalidomide modulates their function. Editorial