ArticleFrontiers in immunology2026
NLRX1 contributes to immunotherapeutic resistance of head and neck squamous cell carcinoma by suppressing type I interferon pathway.
Article in Frontiers in immunology, 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
Background: Head and neck squamous cell carcinoma (HNSCC) faces challenges with limited immune checkpoint inhibitors (ICIs) efficacy. This study identifies NLRX1, highly expressed in HNSCC tumor cells, as a key driver of immune evasion and ICIs' resistance. Methods: This study investigated the role of NLRX1 in HNSCC immune evasion and ICIs resistance. We performed retrospective analyses on patient cohorts to correlate NLRX1 expression with clinical outcomes. Bioinformatic analyses and immunofluorescence staining of human HNSCC tissues were employed to assess associations between immune cell infiltration, gene expression correlations and PD-L1 levels on antigen-presenting cells (APCs). Results: The expression NLRX1 is correlated with unfavorable patient outcomes. NLRX1 promotes tumor progression by modulating the immune microenvironment, not directly affecting tumor cell proliferation. Mechanistically, NLRX1 suppresses the type I interferon (IFN-I) pathway by inhibiting STING expression in HNSCC. Notably, tumor cell-intrinsic NLRX1 negatively correlates with PD-L1 expression on APCs in HNSCC. Conclusions: NLRX1 mediates immune evasion in HNSCC by downregulating STING protein abundance, suppressing the IFN-I pathway, and decreasing PD-L1 expression of APCs. Targeting NLRX1 offers a promising strategy to overcome ICI resistance and improve immunotherapeutic efficacy in HNSCC.
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