Trogocytosis generates acquired regulatory T cells adding further complexity to the dysfunctional immune response in multiple myeloma

Abstract

Trogocytosis, which results in the acquisition of myeloma cell-derived membrane proteins by T cells, and hence generates novel regulatory T cells, adds to the growing list of immune defects of multiple myeloma patients. The increasing complexity of the cancer-associated immune defects must be attentively considered for attempting to improve the so-far unsatisfactory rates of clinical responses to immunotherapy in patients affected by multiple myeloma and other malignancies.

Figure 1. Mechanisms associated with tumor-induced suppression of cytotoxic T cells in multiple myeloma include dysfunctional dendritic cells (DCs) due to plasma cell-derived transforming growth factor β (TGFβ) or interleukin-10 (IL-10), an imbalance between regulatory T cells (Tregs) and T helper 17 (Th17) cells, suppressing T-cell proliferation as well as fracticide or anergy induction as caused by novel Tregs generated by trogocytosis.