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T cells, are key players in mucosal immunity and inflammation, distinguished by their production of IL-17 and related cytokines. In the context of cancer, Th17 cells exhibit extraordinary plasticity-adapting their phenotype and function in response to tumor microenvironmental cues. This review explores how Th17 cells mediate paradoxical roles in tumor biology, promoting either tumor progression or antitumor immunity depending on molecular context. Protumorigenic functions include fostering angiogenesis, chronic inflammation and immune evasion through IL-17-driven recruitment of neutrophils and myeloid-derived suppressor cells. Conversely, Th17 cells can transition into IFNγ-producing Th1-like cells, enhancing cytotoxic T-cell responses and tumor rejection. Key modulators of this plasticity include cytokines (IL-23, IL-12, TGF-β), hypoxia, metabolic shifts and epigenetic reprogramming. We further examine how Th17 plasticity contributes to metastasis, therapy resistance and immune modulation via interactions with tumor-associated macrophages and regulatory T cells. Finally, the review highlights emerging therapeutic strategies that target Th17 pathways through cytokine blockade, metabolic intervention, RORγ modulation and adoptive cell therapy. Understanding Th17 plasticity provides critical insights into tumor immunology and offers novel avenues for cancer immunotherapy.
Sutanto et al. (Thu,) studied this question.