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CD69: from activation marker to metabolic gatekeeper
Open accessAbstract
CD69 is a membrane‐bound, type II C‐lectin receptor. It is a classical early marker of lymphocyte activation due to its rapid appearance on the surface of the plasma membrane after stimulation. CD69 is expressed by several subsets of tissue resident immune cells, including resident memory T (TRM) cells and gamma delta (γδ) T cells, and is therefore considered a marker of tissue retention. Recent evidence has revealed that CD69 regulates some specific functions of selected T‐cell subsets, determining the migration‐retention ratio as well as the acquisition of effector or regulatory phenotypes. Specifically, CD69 regulates the differentiation of regulatory T (Treg) cells as well as the secretion of IFN‐γ, IL‐17, and IL‐22. The identification of putative CD69 ligands, such as Galectin‐1 (Gal‐1), suggests that CD69‐induced signaling can be regulated not only during cognate contacts between T cells and antigen‐presenting cells in lymphoid organs, but also in the periphery, where cytokines and other metabolites control the final outcome of the immune response. Here, we will discuss new aspects of the molecular signaling mediated by CD69 and its involvement in the metabolic reprogramming regulating TH‐effector lineages.
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“CD69 is an activation marker expressed by both effector T cells and tissue-resident (TRM) memory cells [37].”
From The Emerging Fungal Pathogen Candida auris Induces IFNγ to Colonize the Skin (2025) · cites this paper as [37]
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Research works printed but not linked: 2
- 10.1172/JCI200319112 · DOI
- Sanchez‐Diaz R., 2017, Thymus‐derived Treg cell development is regulated by C‐type‐lectin‐mediated BIC/miRNA155 expression, Mol. Cell Biol., 31
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Metadata
- Authors
- Cibrián, D., & Sánchez‐Madrid, F.
- Affiliations
- Instituto de Salud Carlos III (ES)
- Corresponding author
- Sánchez‐Madrid, Francisco
- Venue
- European Journal of Immunology
- Publisher
- Wiley
- Published
- 2017-06
- Volume
- 47
- Issue
- 6
- Pages
- 946-953
- ISSN
- 0014-2980 (ISSN-L)
- 1521-4141
- PMC
- PMC6485631
- OpenAlex
- W2610932550
- Cited by
- 948
- References
- 63
- Citations by year
- 2026: 109 · 2025: 175 · 2024: 150 · 2023: 132 · 2022: 134 · 2021: 101 · 2020: 77 · 2019: 44 · 2018: 22 · 2017: 4
- FWCI
- 4.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- Funders
- Instituto de Salud Carlos III
- Federación Española de Enfermedades Raras
- European Research Council (ERC‐2011‐AdG294340‐GENTRIS)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Galectins and Cancer Biology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- CD69, lymphocyte activation, tissue-resident memory T cells, γδ T cells, Treg differentiation, galectin-1, T cell metabolism, metabolic reprogramming, cytokine production, T cell signaling
- MeSH terms
- CD69 Antigens, Animals, Antigen-Presenting Cells, Antigens, Differentiation, T-Lymphocyte, Cell Differentiation, Gene Expression Regulation, Humans, Lymphocyte Activation, Signal Transduction, Antigens, CD, T-Lymphocyte Subsets, Cytokines, Interleukin-17, Galectins, Lectins, C-Type, T-Lymphocytes, Regulatory
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