ArticleGynecologic oncology reports2026
Local immunosuppressive microenvironment underlies reduced responsiveness to imiquimod treatment in recurrent or residual cervical HSIL.
Article in Gynecologic oncology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Objective: The topical immune modifier imiquimod is used as alternative treatment for cervical high-grade squamous intraepithelial lesions (cHSIL). While its clinical efficacy in primary cHSIL (pcHSIL) is approximately 60%, this is only 33% for recurrent or residual cHSIL (rrcHSIL) due to reasons that are not well understood. Since the immune microenvironment plays a key role in response to imiquimod in pcHSIL, we performed an in depth comparison of the pcHSIL to the rrcHSIL immune microenvironment. Methods: Transcriptome analysis was performed using the nCounter® Human PanCancer IO360™ panel on 6 pcHSIL and 6 rrcHSIL. Multispectral immunofluorescence (13 markers) was used to analyze T- and myeloid-cell composition of pcHSIL (n = 40) and rrcHSIL (n = 10). Differences in pre-treatment immune infiltrates of rrcHSIL were related to clinical response after imiquimod. Results: Transcriptomic analyses revealed lower expression of genes involved in leukocyte activation, immune cell recruitment, T cell engagement, lymphocyte and B cell infiltration in rrcHSIL compared to pcHSIL. Gene set enrichment analysis (GSEA) supported these findings, demonstrating decreased IL2-STAT 5 signaling in rrcHSIL. Immunofluorescence staining results corroborated the transcriptomic data, with rrcHSIL displaying lower intraepithelial infiltration with CD4+(Tbet + ) T cells, and (CD14 + )CD68 + CD163- M1-like macrophages, but higher numbers of CD8+(PD1 + ) T cells and CD68 + CD163 + M2-like macrophages. RrcHSIL non-responders to imiquimod exhibited an even more immunosuppressive microenvironment than complete responders, characterized by increased infiltration of CD4 + FoxP3 + regulatory T cells and (CD14 + )CD68 + CD163 + M2-like macrophages and CD14 + HLADR- monocytic myeloid derived suppressor cells. Conclusions: The limited efficacy of imiquimod in rrcHSIL may be explained by a strong immunosuppressive microenvironment.
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