ArticleProceedings of the National Academy of Sciences of the United States of America2024
cGAS activation in classical dendritic cells causes autoimmunity in TREX1-deficient mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The cGAS-STING Pathway: A Double-Edged Regulator of Neuroinflammation and Myelin Regeneration.Molecular neurobiology · 2026Review
- Autoinflammatory syndromes of STING and TREX1 dysfunction.The Journal of clinical investigation · 2026Review
- The cGAS-STING pathway in pulmonary infectious and sterile inflammation: differences, connections, and therapeutic implications.Frontiers in immunology · 2026Review
- Multilayered interplay between the cGAS-STING pathway and autophagy.Autophagy reports · 2026Review
- Interferons in Autoimmunity: From Loss of Tolerance to Chronic Inflammation.Biomedicines · 2025Review
- Mouse models of type I interferonopathies.Human molecular genetics · 2025Review
- [Research progress on the cGAS-STING signaling pathway in immune-mediated inflammatory diseases in children].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Review
- Induction of Type I Interferon-Dependent Activation and Migration of Inflammatory Dendritic Cells to Local Lymph Nodes by UV Light Exposure.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Detection of cytosolic DNA by the cyclic GMP-AMP (cGAMP) synthase (cGAS)-stimulator of interferon genes (STING) pathway provides immune defense against pathogens and cancer but can also cause autoimmunity when overactivated. The exonuclease three prime repair exonuclease 1 (TREX1) degrades DNA in the cytosol and prevents cGAS activation by self-DNA. Loss-of-function mutations of the TREX1 gene are linked to autoimmune diseases such as Aicardi-Goutières syndrome, and mice deficient in TREX1 develop lethal inflammation in a cGAS-dependent manner. In order to determine the type of cells in which cGAS activation drives autoinflammation, we generated conditional cGAS knockout mice on the Trex1
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