One major complication after solid organ transplantation (SOT) is antibody-mediated rejection (AMR) of the graft by anti-donor HLA antibodies. Modern immunosuppression mainly addresses T cell-mediated rejection, affecting the B-cell alloimmune response only indirectly. B-cell depletion protocols are inefficient in preventing AMR and associated with an increased infection risk, emphasizing the need for a more precise targeting of alloreactive B cells. By the introduction of CARs, T cells can be redirected against various surface antigens and B cells with anti-donor HLA specificity are uniquely characterized by extracellular expression of respective B-cell receptors (BCRs). Using the anti-HLA BCR as target, we redirected T cells towards alloreactive B cells by introducing a novel CAR-like receptor comprising an HLA molecule fused to 4-1BB/CD3ξ signalling domains in order to generate T cells overcoming rejection by antibodies (CORA-T cells). As a proof of concept, CORA-T cells harbouring a receptor with an extracellular truncated HLA-A*02:01 molecule were designed, which was further modified to abrogate CD8 binding. Upon co-cultivation with a B-cell line expressing and releasing anti-HLA-A*02:01 antibodies, CORA-T cells were specifically activated (expression of CD25, CD69, CD137) and released pro-inflammatory cytokines (e.g. IL-2, TNF-α). Moreover, they exhibited cytotoxicity towards target cells and effectively reduced the amount of released anti-HLA-A*02:01 antibody. Our results demonstrate that CORA-T cells are able to specifically recognize and eliminate alloreactive B cells, having the potential to prevent the formation of anti-HLA antibodies. This suggests application of CORA-T cells as an innovative approach to specifically combat AMR to improve long-term graft survival in SOT.