ArticleNature immunology2016
CD69 controls the uptake of L-tryptophan through LAT1-CD98 and AhR-dependent secretion of IL-22 in psoriasis.
Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 75 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
75 citing papers in PubMed, 118 citations in OpenAlex.
- Benzo[a]pyrene vs. Tapinarof: unraveling ligand-specific AHR transcriptional responses in immortalized keratinocytes.Archives of toxicology · 2026Article
- How crosstalk at the immune synapse shapes T cell and dendritic cell biology.Nature reviews. Immunology · 2026Review
- Spatial Transcriptomics Meets Histochemistry: Insights from Glioblastoma as a Model System.Acta histochemica et cytochemica · 2026Review
- Divergent immunometabolic reprogramming in psoriasis and atopic dermatitis: a tale of two inflammatory skin diseases.Frontiers in immunology · 2026Review
- γδ T cells: bridging innate and adaptive immunity in development, tissue residency, and disease.Frontiers in immunology · 2026Review
- LZTR1 regulates epithelial MHC-I expression via NF-κB1 to modulate CD8Cell discovery · 2025Article
- Germinal center formation is resilient to CD69 deletion on T follicular helper cells.Immunology and cell biology · 2025Article
- Epidermal and Dermal T Cells Exhibit Distinct Proteomic Signatures.International journal of molecular sciences · 2025Article
- Rutin ameliorates imiquimod-induced psoriasis-like skin lesions by inhibiting oxidative stress injury and the inflammatory response in mice via the Keap1/Nrf2 signaling pathway.Scientific reports · 2025Article
- Immune-Epithelial Cell Interactions during Epidermal Regeneration, Repair, and Inflammatory Diseases.International journal of stem cells · 2025Review
- T cells in cardiac health and disease.The Journal of clinical investigation · 2025Review
- SLC7A5 regulates tryptophan uptake and PD‑L1 expression levels via the kynurenine pathway in ovarian cancer.Oncology letters · 2025Article
- Skin immune microenvironment in psoriasis: from bench to bedside.Frontiers in immunology · 2025Review
- Functional regulation of cytotoxic T cells by gut microbial metabolites.Gut microbes reports · 2025Article
- Neutrophils Mediate Protection Against Colitis and Carcinogenesis by Controlling Bacterial Invasion and IL22 Production by γδ T Cells.Cancer immunology research · 2024Article
- Comprehensive analysis of disulfidptosis-related genes and the immune microenvironment in heart failure.Frontiers in cell and developmental biology · 2024Article
- Aryl hydrocarbon receptor: current perspectives on key signaling partners and immunoregulatory role in inflammatory diseases.Frontiers in immunology · 2024Review
- Qingxiong Ointment and its Active Ingredient, Shikonin Treat Psoriasis through HIF-1 Signaling Pathway.Current pharmaceutical design · 2024Article
- miR-7 is recruited to the high molecular weight RNA-induced silencing complex in CD8RNA (New York, N.Y.) · 2023Article
- Signaling pathways and targeted therapies for psoriasis.Signal transduction and targeted therapy · 2023Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
The activation marker CD69 is expressed by skin γδ T cells. Here we found that CD69 controlled the aryl hydrocarbon receptor (AhR)-dependent secretion of interleukin 22 (IL-22) by γδ T cells, which contributed to the development of psoriasis induced by IL-23. CD69 associated with the aromatic-amino-acid-transporter complex LAT1-CD98 and regulated its surface expression and uptake of L-tryptophan (L-Trp) and the intracellular quantity of L-Trp-derived activators of AhR. In vivo administration of L-Trp, an inhibitor of AhR or IL-22 abrogated the differences between CD69-deficient mice and wild-type mice in skin inflammation. We also observed LAT1-mediated regulation of AhR activation and IL-22 secretion in circulating Vγ9(+) γδ T cells of psoriatic patients. Thus, CD69 serves as a key mediator of the pathogenesis of psoriasis by controlling LAT1-CD98-mediated metabolic cues.
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Registered trials
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.