ArticleJournal of translational medicine2026
IL-6 regulates the polarization of Dectin-1 macrophages to weaken immune escape in thyroid cancer.
Article in Journal of translational medicine, 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
backgroundImmune evasion is a critical barrier to effective treatment of thyroid carcinoma (TC). Macrophage polarization plays a pivotal role in shaping the tumor microenvironment (TME). This study aimed to elucidate how IL-6 regulates Dectin-1–mediated macrophage polarization and its impact on tumor progression, metabolic reprogramming, and immune remodeling in TC.
methodsSingle-cell RNA sequencing analysis was used to characterize the cellular heterogeneity and communication networks of TCS. Transcriptomic analysis and functional enrichment analysis were performed to identify immunometabolic alterations. In vitro assays included knockdown and overexpression of Dectin-1 in macrophages and co-culture with CAL-62 cells to assess macrophage migration, proliferation, apoptosis, phagocytosis, cytokine secretion, and metabolic activity. In vivo, thyroid cancer mouse models with Dectin-1 knockout or macrophage IL-6 overexpression, with or without ERK pathway regulation (EGF), were established. Phenotypic changes were evaluated by immunofluorescence, immunohistochemistry, Western blot, enzyme-linked immunosorbent assay, hippocampal metabolism test and flow cytometry.
resultsSingle-cell bioinformatics analysis revealed that macrophages are the central hub of immune-epithelial interaction, and Dectin-1 is highly expressed in M1 subsets, which preferentially receive IL-6 signals. Transcriptome bioinformatics analysis showed that Dectin-1 expression was dow-regulated. Functionally, Dectin-1 promotes macrophage migration, phagocytosis, glycolysis, and M1 polarization, while silencing Dectin-1 shifts macrophages to the M2 phenotype, inhibits glycolysis, and reduces antitumor cytokine release. Co-culture experiments indicated that the high expression of Dectin-1 would inhibit the proliferation and migration of TC cells and promote cell apoptosis at the same time, while the activation of IL-6 or ERK could partially reverse this situation. In vivo, Dectin-1 deficiency can enhance tumor proliferation, reduce apoptosis, promote M2-type polarization and decrease the number of CD4+ CD8+ T cells, while ERK pathway activation can eliminate these effects.
conclusionThe IL-6/Dectin-1 axis is a central regulator of macrophage polarization in TC, sustaining an ERK-dependent M1 program that suppresses immune evasion and tumor progression. Targeting IL-6/Dectin-1 signaling rebalances macrophage polarization, enhances effector T-cell responses, and attenuates immune escape, highlighting a potential therapeutic strategy in thyroid carcinoma.
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