ArticleCell death & disease2021
C-type lectin receptor Dectin3 deficiency balances the accumulation and function of FoxO1-mediated LOX-1
Article in Cell death & disease, 2021. 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 19 papers.
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Who cites it
19 citing papers in PubMed, 19 citations in OpenAlex.
- CCR2-overexpressing mesenchymal stromal cell-derived extracellular vesicles loaded with MPA ameliorate lupus nephritis.Journal of nanobiotechnology · 2026Article
- Disparate periphery and lung immune microenvironments induced monocyte-macrophage activation as a key factor in anti-synthetase syndrome-associated interstitial lung disease.Respiratory research · 2026Article
- Therapeutic Remodeling of the Gut Microbiome as a Strategy to Restore Immune Tolerance in Autoimmunity.MicrobiologyOpen · 2026Review
- Study on Immune-Related Genes and Clinical Validation of Acute Myocardial Infarction Based on Bioinformatics.Biochemical genetics · 2026Article
- C-Type lectin receptors as key modulators of intestinal inflammation: insights into IBD pathogenesis and therapy.FEMS microbiology letters · 2026Review
- FOXO1-NMNAT3 axis dysregulation promotes doxorubicin cardiotoxicity: NADRedox report : communications in free radical research · 2025Article
- Immune cells in systemic lupus erythematosus: biology and traditional Chinese medicine therapy.Acta pharmacologica Sinica · 2025Review
- Immunoregulatory iPSC-derived non-lymphoid progeny in autoimmunity and GVHD alloimmunity.Stem cells (Dayton, Ohio) · 2025Review
- FoxO1 Deficiency in Monocytic Myeloid-Derived Suppressor Cells Exacerbates B Cell Dysfunction in Systemic Lupus Erythematosus.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Exploring the molecular mechanism of Tripterygium Wilfordii Hook F in treating systemic lupus erythematosus via network pharmacology and molecular docking.Clinical rheumatology · 2025Article
- Monocyte-macrophage dynamics as key in disparate lung and peripheral immune responses in severe anti-melanoma differentiation-associated gene 5-positive dermatomyositis-related interstitial lung disease.Clinical and translational medicine · 2025Article
- Diverse functions of myeloid-derived suppressor cells in autoimmune diseases.Immunologic research · 2024Review
- CLEC4D as a Novel Prognostic Marker Boosts the Proliferation and Migration of Gastric Cancer via the NF-κB/AKT Signaling Pathway.International journal of general medicine · 2024Article
- Assessing the causal relationship between immune traits and systemic lupus erythematosus by bi-directional Mendelian randomization analysis.Molecular genetics and genomics : MGG · 2023Article
- Myeloid-derived suppressor cells promote the formation of abdominal aortic aneurysms through the IL-3-ICOSL-ICOS axis.BBA advances · 2023Article
- MDSCs participate in the pathogenesis of diffuse pulmonary hemorrhage in murine lupus through mTOR-FoxO1 signaling.Biochemistry and biophysics reports · 2022Article
- Antifungal immunity mediated by C-type lectin receptors may be a novel target in immunotherapy for urothelial bladder cancer.Frontiers in immunology · 2022Article
- IGF1R signalling is a guardian of self-tolerance restricting autoantibody production.Frontiers in immunology · 2022Article
- The Role of C-Type Lectin Receptor Signaling in the Intestinal Microbiota-Inflammation-Cancer Axis.Frontiers in immunology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Recent studies indicate that Toll-like receptors (TLRs) and C-type lectin receptors (CLRs) can function as the signal of pattern recognition receptors, which play a pivotal role in the pathogenesis of the autoimmune disease. Systemic lupus erythematosus (SLE) is a classic autoimmune disease. Previous reports mainly focused on the potential role of TLRs in regulating the development of SLE, but little is known about the role of CLRs in the progression of SLE. Our previous studies showed that the inflammation-mediated accumulation of myeloid-derived suppressor cells (MDSCs) including granulocytic (G-MDSCs) and monocytic (M-MDSCs) participated in the pathogenesis of lupus. Mice deficient in Card9 (the downstream molecule of CLRs) were more susceptible to colitis-associated cancer via promoting the expansion of MDSCs. Whether the abnormal activation of CLRs regulates the expansion of MDSCs to participate in the pathogenesis of lupus remains unknown. In the present study, the expressions of CLRs were examined in both SLE patients and mouse models, revealing the expression of Dectin3 was positively correlated with SLEDAI. Dectin3 deficiency retarded the lupus-like disease by regulating the expansion and function of MDSCs. The mechanistic analysis revealed that Dectin3 deficiency promoted FoxO1-mediated apoptosis of MDSCs. Syk-Akt1-mediated nuclear transfer of FoxO1 increased in Dectin3-deficient MDSCs. Notedly, the accumulation of M-MDSCs mainly decreased in Dectin3
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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.