Despite several reports describing the immunostimulatory properties of Porphyromonas gingivalis–derived FimA, its functional role and underlying mechanism as an adjuvant remain poorly characterized. In this study, we we aimed to investigate whether Porphyromonas gingivalis–derived FimA, a bacterial fimbrial protein could function as an effective adjuvant and to clarify its mechanism of action. To evaluate the immunostimulatory potential of FimA, in vitro analysis using bone marrow-derived dendritic cells (BMDCs) showed that FimA promoted DC maturation in a dose-dependent manner, accompanied by increased expression of co-stimulatory molecules and antigen-presenting markers. In vivo administration of FimA further enhanced the population and activation of splenic DCs and elevated serum levels of pro-inflammatory cytokines. To clarify the molecular basis of these effects, in silico structural modeling and molecular dynamics simulations were performed, revealing that FimA specifically interacts with Toll-like receptor 4 (TLR4), which was consistent with the markedly reduced DC activation observed in TLR4-deficient mice. Comparative analysis demonstrated that P. gingivalis–derived FimA elicited stronger immunostimulatory activity than Escherichia coli–derived FimA. Moreover, co-administration of FimA with the ovalbumin (OVA) antigen significantly enhanced antigen-specific cytotoxic T-lymphocyte (CTL) responses and suppressed B16-OVA tumor growth in vivo. Collectively, these results indicate that FimA acts as a TLR4-dependent immunostimulant with potent adjuvant properties, highlighting its potential as a pathogen-derived candidate for effective cancer immunotherapy.