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Simple Summary  Low expression of  miR-181b  in chronic lymphocytic leukemia (CLL) is linked to progression and cell death resistance. Patients with the progression of the disease show immune dysfunction. We aim at studying whether  miR-181b  is also involved in this process. We demonstrate that  miR-181b  can be increased in CLL cells by crosstalk with CD40L +  T cells, enhancing the maturation of CD8 +  T cells in cytotoxic T lymphocytes (CTL) and, in turn, the anti-tumor cytotoxic T cell response in in vitro and in vivo models. These results demonstrate a role of the  miR-181b  in the immune response against tumor and envisage a therapeutic action of  miR-181b  in a specific milieu surrounding CLL cells.    Abstract  The clinical progression of B cell chronic lymphocytic leukemia (CLL) is associated with immune cell dysfunction and a strong decrease of  miR-181b-5p  ( miR-181b ), promoting the death of CLL cells. Here we investigated whether the reduction of  miR-181b  impairs the immune response in CLL. We demonstrate that activated CD4+ T cells increase  miR-181b  expression in CLL through CD40–CD40L signaling, which enhances the maturation and activity of cytotoxic T cells and, consequently, the apoptotic response of CLL cells. The cytotoxic response is facilitated by a depletion of the anti-inflammatory cytokine interleukin 10, targeted by  miR-181b . In vivo experiments in NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ mice confirmed that  miR-181b  promotes the apoptotic death of CLL cells only when functional T cells are restored. Overall, our findings suggest that the reinstatement of  miR-181b  in CLL cells could be an exploitable adjuvant therapeutic option for the treatment of CLL.

Enhanced Expression of miR-181b in B Cells of CLL Improves the Anti-Tumor Cytotoxic T Cell Response