ArticleAutophagy2018
TNFAIP3-DEPTOR complex regulates inflammasome secretion through autophagy in ankylosing spondylitis monocytes.
Article in Autophagy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed, 62 citations in OpenAlex.
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- A20 Attenuates Inflammatory Injury in Bovine Endometrial Epithelial Cells Through Autophagy-Mediated NLRP3 Inflammasome Inactivation.Animals : an open access journal from MDPI · 2025Article
- The Role of A20 in Cancer: Friend or Foe?Cells · 2025Review
- A novel missense variant in TNFAIP3 associated with autoimmunity reveals the contribution of STAT1/mTOR pathways.Clinical and experimental immunology · 2025Article
- Deptor protects against myocardial ischemia-reperfusion injury by regulating the mTOR signaling and autophagy.Cell death discovery · 2024Article
- Exploring T Cell and NK Cell Involvement in Ankylosing Spondylitis Through Single-Cell Sequencing.Journal of cellular and molecular medicine · 2024Article
- A20 Alleviates the Inflammatory Response in Bovine Endometrial Epithelial Cells by Promoting Autophagy.Animals : an open access journal from MDPI · 2024Article
- Article
- The Complexity of Being A20: From Biological Functions to Genetic Associations.Journal of clinical immunology · 2024Review
- CD_99 G1 neutrophils modulate osteogenic differentiation of mesenchymal stem cells in the pathological process of ankylosing spondylitis.Annals of the rheumatic diseases · 2024Article
- Osteoblast-specific down-regulation of NLRP3 inflammasome by aptamer-functionalized liposome nanoparticles improves bone quality in postmenopausal osteoporosis rats.Theranostics · 2024Article
- Metformin inhibits EV71‑induced pyroptosis by upregulating DEP domain‑containing mTOR‑interacting protein.Experimental and therapeutic medicine · 2023Article
- A20 interacts with mTORC2 to inhibit the mTORC2/Akt/Rac1 signaling axis in hepatocellular carcinoma cells.Cancer gene therapy · 2023Article
- Novel Autophagy-Related Blood Biomarkers Associated with Immune Cell Infiltration in Ankylosing Spondylitis.Pharmacogenomics and personalized medicine · 2023Article
- Targeting inflammasome-dependent mechanisms as an emerging pharmacological approach for osteoarthritis therapy.iScience · 2022Review
- NLRP3 inflammasome up-regulates major histocompatibility complex class I expression and promotes inflammatory infiltration in polymyositis.BMC immunology · 2022Article
- Article
- A20 attenuates pyroptosis and apoptosis in nucleus pulposus cells via promoting mitophagy and stabilizing mitochondrial dynamics.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- VSIG4 Attenuates NLRP3 and Ameliorates Neuroinflammation via JAK2-STAT3-A20 Pathway after Intracerebral Hemorrhage in Mice.Neurotoxicity research · 2022Article
- Advances in the Study of the Ubiquitin-Editing Enzyme A20.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Ankylosing spondylitis (AS) is a chronic autoimmune inflammatory disease with severe inflammatory symptoms in the axial skeleton. The cause of ankylosing spondylitis is unknown. TNFAIP3, also named A20, uses ubiquitin-related functions to regulate immune activation, deficiency of which is highly related to autoimmune disease. However, the role of TNFAIP3 in human AS has not been reported. Our objective was to study the role and mechanism of TNFAIP3 in ankylosing spondylitis. TNFAIP3 expression on different types of immunocytes from AS peripheral blood was measured by flow cytometry. In vitro, monocytes were transfected with a TNFAIP3 shRNA lentivirus, and IL6 and IL1B activation was tested using real-time PCR and ELISA. The novel interaction complex TNFAIP3-DEPTOR was determined through GST pull-down, yeast two-hybrid system, confocal microscopy, and co-immunoprecipitation. Transmission electron microscopy, the RFP-GFP-LC3 adenovirus, and LC3 expression were used for autophagy detection. Here, we show that TNFAIP3 expression in AS peripheral blood non-classical monocytes was decreased. In normal monocytes, TNFAIP3 induced autophagy, which restricted inflammasome activation to the early stage of LPS stimulation. Zinc-finger domains of TNFAIP3 were able to interact and stabilize DEPTOR. TNFAIP3 and DEPTOR together rapidly promoted autophagy after LPS treatment to prevent NLRP3 inflammasome formation. Finally, TNFAIP3 and DEPTOR deficiency in AS non-classical monocytes facilitated inflammasome activation. Our study indicates that TNFAIP3-DEPTOR complex-induced early-onset autophagy is vital for immune inhibition in autoimmune disease.
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Registered trials
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