ArticleScience translational medicine2020
Mannose receptor (CD206) activation in tumor-associated macrophages enhances adaptive and innate antitumor immune responses.
Article in Science translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers, 1 of them a synthesis that pooled it.
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Who cites it
219 citing papers in PubMed, 1 synthesis or guideline pooled it, 408 citations in OpenAlex.
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- Engineering macrophages for cancer immunotherapy: emerging insights and therapeutic potential.npj biomedical innovations · 2026Review
- Targeted drug delivery strategies for oral cancer: the role of liposomes in drug delivery systems.Biomedical engineering online · 2026Review
159 more citing papers are in PubMed but not listed here.
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43 authors at 11 institutions in 2 countries.
Funding
Abstract
Solid tumors elicit a detectable immune response including the infiltration of tumor-associated macrophages (TAMs). Unfortunately, this immune response is co-opted into contributing toward tumor growth instead of preventing its progression. We seek to reestablish an antitumor immune response by selectively targeting surface receptors and endogenous signaling processes of the macrophage subtypes driving cancer progression. RP-182 is a synthetic 10-mer amphipathic analog of host defense peptides that selectively induces a conformational switch of the mannose receptor CD206 expressed on TAMs displaying an M2-like phenotype. RP-182-mediated activation of this receptor in human and murine M2-like macrophages elicits a program of endocytosis, phagosome-lysosome formation, and autophagy and reprograms M2-like TAMs to an antitumor M1-like phenotype. In syngeneic and autochthonous murine cancer models, RP-182 suppressed tumor growth, extended survival, and was an effective combination partner with chemo- or immune checkpoint therapy. Antitumor activity of RP-182 was also observed in CD206
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