ReviewImmunoTargets and therapy2026
A Review of Aryl Hydrocarbon Receptor-Mediated Immune Regulation in Cutaneous Squamous Cell Carcinoma Progression.
Review in ImmunoTargets and therapy, 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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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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Authors and funding
11 authors.
Funding
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Abstract
The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that was initially discovered for its role in mediating the toxicity of environmental pollutants such as dioxins. Recent studies have demonstrated that AhR plays significant roles in various physiological and pathological processes, including immune regulation and tumor development. Cutaneous squamous cell carcinoma (cSCC), the second most common skin malignancy, is closely associated with the immune microenvironment. This review systematically outlines the structure, function, and signaling pathways of AhR, as well as its role in the immune system, with a focus on how AhR influences the progression of cSCC by regulating the functions of various immune cells, including T cells, dendritic cells, macrophages, and myeloid-derived suppressor cells. In particular, this review highlights the central role of the "tryptophan-kynurenine-AhR" axis, along with AhR-mediated regulation of immune checkpoints (such as PD-1/PD-L1, CTLA-4, and TIM-3), its crosstalk with inflammatory signaling pathways (including NF-κB, STAT3, and TGF-β), and the impact of AhR on antigen presentation and immunoediting. Furthermore, it discusses the role of AhR ligands in cSCC and the potential of targeting AhR for therapy, providing a novel theoretical foundation and strategic insights for the immunotherapy of cSCC. This review systematically summarizes the immunomodulatory mechanisms of AhR, integrating findings from studies specific to cSCC and those from other tumor types. It should be noted that some mechanistic evidence is derived from non-cSCC research models, and its applicability to cSCC requires further validation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.