Fig. 2

Cell therapies for renal cell carcinoma. A Allogeneic hematopoietic stem cell transplantation, presenting acute and chronic graft versus host disease (GvHD) with high transplant-related mortality; B Interleukin-2 (IL-2) and IL-2 receptor (IL-2R) variants, where mutants allowing only hIL-2Rβ activation on adoptive T cells but not the hIL-2Rα prevent T cells differentiation into Tregs and induce expansion of effector T cells against the tumor; C T cell receptor gene-modified T cells (TCR-T), which is consisted of a chimeric switch receptor (CSR) combining a ligand-binding domain (e.g., PD-1) with an alternative signaling domain (CD28) able to prevent T cell exhaustion and improve expansion; D Chimeric antigen receptor (CAR) T cells, and E CAR natural killer (NK) cells, both expressing engineered receptors designed against one or more antigens allowing immune cells activation against the tumor; F Lymphokine-activated killer (LAK) cells, that are T and NK cells, mainly expressing NK markers. Despite some efficiency against RCC metastasis, LAK cell therapy has been replaced by more specific cell-based immunotherapies; G γδ T cells, a subset of T cells with non-MHC‐restricted cytotoxic activity. These cells can be engineered for adoptive therapies, and the PD-1/PD-L1 axis does not abrogate their function; H Dendritic cell vaccination, where autologous DCs pulsed with peptides or tumor lysate-derived proteins can stimulate the generation of cytotoxic T cells in cancer patients. Created with BioRender.com