ArticleiScience2026
Inflammatory CD4
Article in iScience, 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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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.
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Authors and funding
9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis and lipid peroxidation are associated with inflammatory and pathogenic conditions. However, cell-specific mechanisms and functions are not fully understood. Cysteine is an essential amino acid for T cell activation and proliferation and is required to synthesize glutathione, the most abundant antioxidant molecule in cells. Cysteine is predominantly produced intracellularly after uptake of its oxidized form (cystine) by SLC7A11. In this study, we provide a detailed analysis of lipid peroxidation in human T cells and analyzed functional consequences in the chronic inflammatory condition of childhood arthritis. We found that healthy peripheral blood CD4 T cells are not fully dependent on SLC7A11 expression and cystine uptake to prevent ferroptotic cell death, most likely by switching to ASCT1-mediated cysteine uptake. T cells from patients with JIA have a high ASCT1 expression, which most likely prevents exaggerated lipid peroxidation and enables them to maintain their inflammatory phenotype in challenging environments such as inflamed joints.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.