Following subcutaneous implantation, the murine lymphoma E.G7 [a variant of EL‐4, transfected with the chicken ovalbumin (OVA) gene] up‐regulates the CD4 molecule. We previously showed that the administration of an anti‐CD4 monoclonal antibody (mAb) to EG.7‐bearing mice leads to a rapid and complete regression of large established tumors. This tumor regression was shown to require both CD8⁺ cells and functional Fcγ receptors (FcγR), as it failed to occur in mice depleted of CD8 cells, or mice genetically deficient in FcγRI/III (γ^{− / −} mice). Using adoptive transfer, we now show that the FcγR⁺ cells required for this regression are the CD11b⁺ (phagocytic) cells. Furthermore, experiments using peptide tolerization demonstrated that the critical CD8 CTL population in this model is tumor specific. Analysis of tumors at various stages of regression revealed a massive CD11b⁺ FcγR⁺ and a marginal CD8 infiltration. In the presence of the CTL determinant OVA‐8 on tumor cells and of the antitumor mAb, this CD8 infiltration became remarkable, and correlated with tumor regression. These results identify the specific cellular effectors essential for the mAb‐mediated tumor regression, and suggest that FcγR‐activated macrophages induced an expansion of tumor‐eliminating CTL in situ.