ArticleJournal for immunotherapy of cancer2026
Adipocyte-derived LTB4 programs human NKG2A
Article in Journal for immunotherapy of cancer, 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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34 authors.
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Abstract
backgroundThe peritumoral microenvironment has emerged as a key role in affecting tumor invasion and immunotherapy responses. In adipose-enriched tumors, such as breast cancer (BC), peritumoral adipose tissue (PA) harbors unconventional immune populations, yet its immunological functions remain poorly understood. In particular, how adipocyte regulate innate-like lymphocytes, such as γδ T cells, remains unclear.
methodsWe performed single-cell RNA sequencing and spatial profiling of paired specimens from patients with BC. Integrated multi-omics analyses, immunofluorescence staining, human γδ T-cell expansion assays, functional assays, and in vivo models were used to define the immune cell states and evaluate the impact of lipid mediator leukotriene B4 (LTB4) on γδ T-cell activation and signaling. Clinical correlations were assessed using our cohort and patient datasets.
resultsWe identified a previously unrecognized population of NKG2A
conclusionsThese findings redefine PA as an active immunological niche that programs γδ T-cell immunity through adipocyte-derived LTB4 signaling. Our study identifies NKG2A
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