ArticleThe Journal of clinical investigation2016
Collectin-11 detects stress-induced L-fucose pattern to trigger renal epithelial injury.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 134 citations in OpenAlex.
- Back-table intra-arterial administration of C1 esterase inhibitor to deceased donor kidney allografts improves posttransplant allograft function: Results of a randomized double-blind placebo-controlled clinical trial.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025Trial
- Trial
- Advances in Complement Research: from Pathophysiology to Precision Medicine.Physiology (Bethesda, Md.) · 2026Review
- Complement activation in kidney transplantation.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026Review
- L-Fucose: a dietary sugar with multifaceted potential in the biology and therapy of cancer.Nature reviews. Cancer · 2026Review
- Collectin-11 regulates osteoclastogenesis and bone maintenance via a complement-dependent mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage.Frontiers in immunology · 2026Review
- Rationale for Targeting Complement to Mitigate Renal Transplant Ischemia-Reperfusion Injury.Journal of the American Society of Nephrology : JASN · 2026Review
- Glycan recognition by collectin-11 drives SARS-CoV-2 infectivity and membrane injury of respiratory epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- PS77: a novel peptide with α-helical structure for targeted anti-inflammatory therapy in biomaterials design.Immunologic research · 2025Article
- Friend or foe: assessing the value of animal models for facilitating clinical breakthroughs in complement research.The Journal of clinical investigation · 2025Review
- Role of intrarenal complement production in kidney transplantation.Clinical kidney journal · 2025Review
- Targeting the complement lectin pathway with a highly specific MASP-2 inhibitor protects against renal ischemia-reperfusion injury.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Adaptation and conservation of CL-10/11 in avian lungs: implications for their role in pulmonary innate immune protection.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Article
- Pilot Study of Sodium-Glucose Cotransporter 2 Inhibitor Empagliflozin Shows Reduced Intrarenal Complement Activation in Patients With Diabetes and CKD.Kidney international reports · 2025Article
- Candidiasis: Insights into Virulence Factors, Complement Evasion and Antifungal Drug Resistance.Microorganisms · 2025Review
- Collectin-11 promotes fibroblast proliferation and modulates their activation status and extracellular matrix synthesis.Frontiers in immunology · 2025Article
- Immune Landscape in Kidney Transplantation.Journal of inflammation research · 2025Review
- Characterization of a Long-Acting Anti-Human MASP-2 Antibody for the Treatment of Complement-Related Diseases.Journal of inflammation research · 2025Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Physiochemical stress induces tissue injury as a result of the detection of abnormal molecular patterns by sensory molecules of the innate immune system. Here, we have described how the recently discovered C-type lectin collectin-11 (CL-11, also known as CL-K1 and encoded by COLEC11) recognizes an abnormal pattern of L-fucose on postischemic renal tubule cells and activates a destructive inflammatory response. We found that intrarenal expression of CL-11 rapidly increases in the postischemic period and colocalizes with complement deposited along the basolateral surface of the proximal renal tubule in association with L-fucose, the potential binding ligand for CL-11. Mice with either generalized or kidney-specific deficiency of CL-11 were strongly protected against loss of renal function and tubule injury due to reduced complement deposition. Ex vivo renal tubule cells showed a marked capacity for CL-11 binding that was induced by cell stress under hypoxic or hypothermic conditions and prevented by specific removal of L-fucose. Further analysis revealed that cell-bound CL-11 required the lectin complement pathway-associated protease MASP-2 to trigger complement deposition. Given these results, we conclude that lectin complement pathway activation triggered by ligand-CL-11 interaction in postischemic tissue is a potent source of acute kidney injury and is amenable to sugar-specific blockade.
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