Chronic Lymphocytic Leukaemia (CLL) is a lymphoproliferative cancer characterised by accumulation of mature CD5⁺ B-lymphocytes in the blood, bone marrow and secondary lymphoid organs. CLL cells escape anti-tumour immune surveillance by promoting immune dysfunction through the release of CLL-derived soluble factors, or direct cell-cell contact involving inhibitory receptors. Immune dysfunction in CLL includes hypogammaglobulinemia and defects in cell-mediated immunity. As a consequence, CLL patients show an increased susceptibility to infections, which is exacerbated by current treatments. Moreover, CLL cells create a supportive microenvironment in lymphoid tissues, where neighbouring cells produce chemokines, cytokines and survival factors such as BAFF and APRIL. Using a mouse model of CLL (TCL1-Tg), we show that loss of TACI (a receptor for BAFF and APRIL) within leukemic cells, ameliorates immune dysfunction. TACI-deficient TCL1-Tg mice show restored levels of IL-10, an immunosuppressive cytokine upregulated in patients with CLL and in TACI-sufficient TCL1-Tg mice. TACI^-/- TCL1-Tg mice exhibit a normalised T-cell compartment compared with TACI^+/+ TCL1-Tg, with corrected numbers of naïve CD8⁺ T cells and Tregs. Moreover, TACI-deficient CLL cells express lower levels of the inhibitory receptor PD-L1, which binds to PD-1 on T cells and suppresses T-cell function. Lastly, immunoglobulin levels, which are dramatically reduced in TACI^+/+ TCL1-Tg mice, were restored in TACI^-/- TCL1-Tg mice. Together, our results suggest that TACI blockade could represent a new immunotherapeutic approach to enhance immune function in patients with CLL.