Abstract
Immunotherapy represents a promising new avenue for the treatment of multiple myeloma (MM) patients, particularly with the availability of Monoclonal Antibodies (mAbs) as anti-CD38 Daratumumab and Isatuximab and anti-SLAM-F7 Elotuzumab. Although a clear NK activation has been demonstrated for Elotuzumab, the effect of anti-CD38 mAbs on NK system is controversial. As a matter of fact, an initial reduction of NK cells number characterizes Daratumumab therapy, limiting the potential role of this subset on myeloma immunotherapy. In this paper we discuss the role of NK cells along with anti-CD38 therapy and their implication in plasma cell dyscrasias, showing that mechanisms triggered by anti-CD38 mAbs ultimately lead to the activation of the immune system against myeloma cell growth.
Highlights
Natural killer cells are a group of innate lymphoid cells (ILCs) with strong cytotoxic function against stressed cells, such as virus-infected cells or tumor cells
Granzymes regulate the production of proinflammatory cytokines (IL-1β) by a mechanism dependent on caspase-1 [7]. Another process by which NK cells mediate killing of target cells involves the activation of death receptors of the tumor necrosis factor receptor (TNFR) superfamily that are expressed on the target cells
NK cells play a crucial role in immunotherapy against myeloma cells
Summary
Natural killer cells are a group of innate lymphoid cells (ILCs) with strong cytotoxic function against stressed cells, such as virus-infected cells or tumor cells. They represent 5–15% of human peripheral blood mononuclear cells (PBMC) and tissue-resident NK cells can be found in the skin, spleen, liver, lungs, and other organs under physiological conditions [1]. The downregulation of CD56 is associated with the acquisition of a high cytotoxic potential and this reflects the distinct physiological roles of the two NK cell subsets: CD56bright population is specialized in the production of inflammatory cytokines and chemokines, while the cytotoxic function resides primarily in CD56dim cells [3]. The different functions of CD56bright and CD56dim populations reflect the presence of distinct NK receptors and other molecules on the surface of the two subsets including CD16, which is expressed on most CD56dim cells and in a limited subset of CD56bright cells
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