Anti-tumor immune responses to lymphoid malignancies are modulated by co-stimulatory and co-inhibitory pathways. Our group previously characterized the recurrent genetic alterations in primary diffuse large B-cell lymphomas (DLBCL) and identified frequent inactivating mutations or copy loss of the CD70co-stimulatory ligand in these tumors. CD70 co-stimulation of CD27 +T cells induces antigen-dependent T-cell expansion and immune surveillance of normal and malignant B cells. Given the frequent combination of CD70and BCL6alterations in our human DLBCL series, we investigated the consequences of CD70deficiency ( Cd70-/-) in a murine model of BCL6-driven lymphomagenesis ( Bcl6tg/+).