ArticleNature communications2026
Palmitic acid-triggered B7H3 palmitoylation promotes immune escape.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- CD112 Lactylation Drives Dual Immune Evasion From CD8+ T Cells and NK Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Acyl-CoA thioesterases and their derived lipid mediators: linking Acyl-CoA metabolic reprogramming to the tumor microenvironment.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer responds poorly to immune checkpoint blockade in most patients with microsatellite-stable (MSS) tumors, highlighting the need for alternative targets. B7H3 (CD276) is an immune checkpoint protein that is frequently overexpressed in tumors, but how it is maintained at high protein levels is unclear. Here we show that palmitic acid (PA) promotes B7H3 palmitoylation by the palmitoyltransferase ZDHHC24 at cysteine 496. This modification prevents B7H3 from binding to sequestosome 1 (SQSTM1, also called p62), limiting autophagic degradation and stabilizing B7H3, which suppresses CD8
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