ArticleImmunology2005
Glycation of CD59 impairs complement regulation on erythrocytes from diabetic subjects.
Article in Immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Glycation of the complement regulatory protein CD59 is a novel biomarker for glucose handling in humans.The Journal of clinical endocrinology and metabolism · 2014Trial
- A specific and sensitive assay for blood levels of glycated CD59: a novel biomarker for diabetes.American journal of hematology · 2013Trial
- Hemorheological Alterations as a Driver of Microangiopathy in Diabetic Kidney Disease-The Role of Erythrocyte.International journal of molecular sciences · 2026Review
- The Relationship of the Plasma Glycated CD59 Level with Microvascular Complications in Diabetic Patients and Its Evaluation as a Predictive Marker.Journal of clinical medicine · 2025Article
- Regulation of the terminal complement cascade in adipose tissue for control of its volume, cellularity, and fibrosis.Obesity (Silver Spring, Md.) · 2025Review
- Exploring Structural and Molecular Features of Sciatic Nerve Lesions in Diabetic Neuropathy: Unveiling Pathogenic Pathways and Targets.Diabetes · 2025Article
- Proteomic Profiling of Endothelial Cell Secretomes After Exposure to Calciprotein Particles Reveals Downregulation of Basement Membrane Assembly and Increased Release of Soluble CD59.International journal of molecular sciences · 2024Article
- Glycated CD59 is a potential biomarker for gestational diabetes mellitus.Frontiers in endocrinology · 2024Article
- The Role of Early Pregnancy Maternal pGCD59 Levels in Predicting Neonatal Hypoglycemia-Subanalysis of the DALI Study.The Journal of clinical endocrinology and metabolism · 2022Observational
- Long-term peritoneal dialysate exposure modulates expression of membrane complement regulators in human peritoneal mesothelial cells.Frontiers in medicine · 2022Article
- Complement regulation in tenocytes under the influence of leukocytes in an indirect co-culture model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- Plasma glycated CD59 (gCD59), a novel biomarker for the diagnosis, management and follow up of women with Gestational Diabetes (GDM) - protocol for prospective cohort study.BMC pregnancy and childbirth · 2020Article
- Article
- The eye as a complement dysregulation hotspot.Seminars in immunopathology · 2018Review
- Targeted complement inhibition as a promising strategy for preventing inflammatory complications in hemodialysis.Immunobiology · 2012Review
- Modulation of CD59 expression by restrictive silencer factor-derived peptides in cancer immunotherapy for neuroblastoma.Cancer research · 2008Article
- Myasthenia gravis thymus: complement vulnerability of epithelial and myoid cells, complement attack on them, and correlations with autoantibody status.The American journal of pathology · 2007Article
- Contributions of inflammatory processes to the development of the early stages of diabetic retinopathy.Experimental diabetes research · 2007Review
- Analysis of the promoters and 5'-UTR of mouse Cd59 genes, and of their functional activity in erythrocytes.Genes and immunity · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes is associated with anaemia. Although the underlying mechanisms remain unclear, the accompanying reticulocytosis implies that erythrocyte lifespan in the circulation is shortened. Among the factors that permit prolonged survival of erythrocytes are the membrane complement regulators. In conditions such as paroxysmal nocturnal haemoglobinuria, where erythrocyte expression of these regulators is reduced, erythrocyte survival is compromised and anaemia follows. Recent in vitro evidence indicates that one of the key membrane complement regulators, CD59, is inactivated by glycation in the presence of high concentrations of glucose or other glycating sugars. To ascertain whether glycation-induced inactivation of CD59 occurrs in vivo we examined CD59 surface expression and function on erythrocytes from a cohort with poorly controlled type 1 diabetes (hyperglycaemic) and from matched normoglycaemic controls. Although expression of CD59, assessed using polyclonal anti-CD59 antiserum, was similar in the two groups, erythrocytes from hyperglycaemic individuals were more susceptible to lysis by complement, entirely as a result of the loss of functional CD59. These data implicate glycation-induced inactivation of CD59 as a factor contributing to anaemia in type 1 diabetes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.