As previous studies have confirmed that FimH and PapG, adhesion molecules of E. coli, are involved in the activation of immune cells, bacterial adhesion molecules may be involved in immune activation in addition to their function in adhering to epithelial cells. Porphyromonas gingivalis (P. gingivalis), the causative agent of periodontitis, also has an adhesion molecule called Mfa1, but the immune activation ability of this protein is still insufficiently studied. Therefore, in this study, we evaluated the immune cell activity, especially the activity of dendritic cells (DCs) and T cells, by Mfa1 of P. gingivalis, and further confirmed the anticancer effect by combined treatment with anti-programmed death-ligand 1 (PD-L1) antibody, an immune anticancer agent. Treatment of bone marrow-derived DCs with Mfa1 induced robust changes in dendritic morphology, increased expression of surface activation markers, and upregulated secretion of pro-inflammatory cytokines. Administration of Mfa1 to C57BL/6 mice increased the proportion and number of splenic DCs and its subsets together with upregulation of the expression of C-C chemokine receptor type 7, indicating DC migration and maturation. Furthermore, Mfa1 treatment elevated co-stimulatory and MHC molecules in splenic DC subsets, and increased production levels of pro-inflammatory cytokine in the serum by TLR2 stimulation. In addition, Mfa1 promoted increased levels of intracellular production of IFN-γ and TNF-α in CD4⁺ and CD8⁺ T cells. Finally, in a Lewis lung carcinoma model, Mfa1 enhanced the antitumor efficacy of anti–PD-L1 antibody. Thus, Mfa1 may serve as a potential immunostimulatory adjuvant to enhance cancer immunotherapy.