ArticleiScience2025
Macrophage fatty acid metabolism under chronic hypoxia shapes γδ T cell recruitment via CCL22.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- γδ T cells and cancer.The Journal of clinical investigation · 2026Review
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia in solid tumors is associated with poor outcomes because of metabolic adaptations that support tumor cell survival and alter immune cell function. However, the metabolic and phenotypic adaptations of macrophages (MФs) to chronic hypoxia (CH) remain unclear. This study identifies impaired activity of the oxygen-dependent enzyme stearoyl-CoA desaturase 1 (SCD1) as a driver of altered fatty acid (FA) metabolism in MФs under CH. SCD1 deletion enhanced pro-inflammatory gene expression while suppressing the production of the chemokine CCL22. We propose that attenuated SCD1 activity and an altered saturated fatty acids (SFA)/monounsaturated fatty acids (MUFA) ratio impair the function of the transcription factor HNF4α, thereby affecting the expression of inflammatory genes such as CCL22. Reduced CCL22 levels, in turn, impaired γδ T cell recruitment. Accordingly, CCL22 expression in non-small cell lung cancer patients correlated positively with γδ T cell frequency and patient survival. These findings highlight the immunometabolic role of SCD1 in the hypoxic tumor microenvironment.
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