ArticleFrontiers in immunology2026
pAc/Emm55 increases anti-melanoma immunity via TLR2 signaling in dendritic cells and improves checkpoint blockade efficacy.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: pAc/Emm55 (IFx-Hu2.0) is a plasmid DNA therapy encoding a Methods: B16 melanoma tumor-bearing mice were treated intratumorally with pAc/Emm55 alone and/or intraperitoneally with PD-1, CTLA-4, or LAG-3 blockade and monitored for tumor growth. Antibodies against Emm55 and melanoma cells (B16 or YUMM) were quantified by flow cytometry. Bone marrow-derived dendritic cells (BMDCs) from WT, MyD88 KO, TLR2 KO, or TLR7 KO mice were assessed for antigen uptake, OVA cross-presentation, and OT-I priming after pulsing with cell lysates from Emm55- or empty-transfected melanoma cells. Tumor immune infiltration by CD8 and CD11c cells were evaluated by immunohistochemistry. Results: IFx-Hu2.0 significantly reduced tumor growth, correlating with increased intratumoral CD8 Conclusions: Emm55 facilitates the TLR2-MyD88 pathway in DCs and subsequent IFN-γ production by OT-I CD8 T cells. Combining intratumoral IFx-Hu2.0 with PD-1 blockade improves tumor control, supporting clinical evaluation of this strategy as also suggested by the first-in-human clinical trial of IFx-Hu2.0.
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