ArticleFrontiers in immunology2024
Blocking S100A9-signaling is detrimental to the initiation of anti-tumor immunity.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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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Who cites it
6 citing papers in PubMed.
- Review
- Discovery of a non-canonical TREM2-S100A9 axis that drives pro-tumorigenic macrophage polarization and sensitizes ovarian clear cell carcinoma to IL-17 blockade.Cell death discovery · 2026Article
- S100A8/A9 as a key player in colorectal cancer: from diagnosis to therapeutic targeting.Frontiers in pharmacology · 2026Review
- Neural stem cell-delivered oncolytic virus via intracerebroventricular administration enhances glioblastoma therapy and immune modulation.Journal for immunotherapy of cancer · 2025Article
- Paquinimod-hydrogel hybrid microneedle array patch alleviates hypertrophic scar via inhibiting M1 polarization.Bioengineering & translational medicine · 2025Article
- The immunosuppressive role of MDSCs in HCC: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100A9, a multifunctional protein mainly expressed by neutrophils and monocytes, poses an immunological paradox. In virus infections or sterile inflammation, it functions as an alarmin attracting innate immune cells, as well as mediating proinflammatory effects through TLR4 signaling. However, in cancer, S100A9 levels have been shown to associate with poor prognosis and lack of response to immunotherapy. Its expression by myeloid cells has been related to an immune suppressive phenotype, the so-called myeloid derived suppressor cells (MDSCs). Targeting S100A9 in cancer has therefore been proposed as a potential way to relieve myeloid-mediated immune suppression. Surprisingly, we found that blocking the extracellular TLR4 signaling from S100A9 using the inhibitor Paquinimod, resulted in increased tumor growth and a detrimental effect on anti-PD-L1 efficacy in the CT26 tumor model. This effect was caused by a reduction in the tumor immune infiltration to about half of untreated controls, and the reduction was made up of a 5-fold decrease in Ly6C
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Registered trials
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