ArticleFrontiers in immunology2025
OX-40 signaling promotes tumorigenesis in CTCL by regulating ERK activation.
Article in Frontiers in immunology, 2025. 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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Who cites it
1 citing paper in PubMed.
- The OX40-OX40L Co-Stimulatory Pathway as a Shared Driver of Immune Persistence in Skin and Airway Inflammation.Clinical reviews in allergy & immunology · 2026Review
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8 authors.
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Abstract
Introduction: In Cutaneous T-cell Lymphoma (CTCL), T cells can be activated either by cytokines produced by malignant T cells or through immunological synapses, such as the interaction between OX-40 and OX-40L on dendritic cells. Both are co-expressed in tumor cells in Mycosis fungoides/Sézary syndrome and correlate with disease severity markers. Using a model of spontaneous metastasis in chick embryos, the present study aimed to determine the functional role of OX-40 in CTCL and assess its potential as a therapeutic target. Methods: OX-40 knockout MyLa and SeAx CTCL cells using CRISPR-Cas9 were engrafted onto the chorioallantoic membrane of chick embryos. We assessed tumor growth, dissemination, and TME modulation in the presence or absence of macrophages. Transwell-based transendothelial migration assays and co-culture experiments were performed to further explore the interactions between CTCL cells and macrophages. Angiogenesis and lymphangiogenesis have also been investigated. Results: OX-40 expression promoted intravasation, metastasis, and cytokine secretion, and increased M2 macrophages. Additionally, it restores transendothelial migration and dissemination in the presence of M2 macrophages, possibly through ERK activation. Co-culture experiments revealed that OX-40 promoted a Th2 cytokine profile in CTCL, correlating with M2 macrophages in xenografts. Although OX-40 did not affect angiogenesis in this model, it promoted lymphangiogenesis via VEGF-C expression. Discussion: Using the CTCL spontaneous metastasis model in chick embryos, we demonstrated that OX-40 regulates the TME to promote M2 increase, lymphangiogenesis, CAM intravasation, and metastasis. Therefore, the
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