ArticleThe Journal of experimental medicine1995
Transient perturbation of endothelial integrity induced by natural antibodies and complement.
Article in The Journal of experimental medicine, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 229 citations in OpenAlex.
- Modeling antithymocyte globulin-induced microvasculopathy using human iPSC-derived vascularized liver organoids.Cell reports. Medicine · 2025Article
- Functional Roles of the Complement Immune System in Cardiac Inflammation and Hypertrophy.International journal of molecular sciences · 2025Review
- Podocyte Pathogenic Bone Morphogenetic Protein-2 Pathway and Immune Cell Behaviors in Primary Membranous Nephropathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Accommodation in allogeneic and xenogeneic organ transplantation: Prevalence, impact, and implications for monitoring and for therapeutics.Human immunology · 2023Article
- Can Heart Valve Decellularization Be Standardized? A Review of the Parameters Used for the Quality Control of Decellularization Processes.Frontiers in bioengineering and biotechnology · 2022Review
- Complement Activation Contributes to the Pathophysiology of Shiga Toxin-Associated Hemolytic Uremic Syndrome.Microorganisms · 2019Review
- Accommodation in ABO-incompatible organ transplants.Xenotransplantation · 2018Review
- Kidney xenotransplantation.Kidney international · 2014Review
- Interleukin-4 induces up-regulation of endothelial cell claudin-5 through activation of FoxO1: role in protection from complement-mediated injury.The Journal of biological chemistry · 2014Article
- Identification of the tetraspanin CD82 as a new barrier to xenotransplantation.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- STEC-HUS, atypical HUS and TTP are all diseases of complement activation.Nature reviews. Nephrology · 2012Review
- Human leukocyte antigen antibody incompatible renal transplantation.Indian journal of nephrology · 2012Article
- B cells in cardiac transplants: from clinical questions to experimental models.Seminars in immunology · 2012Review
- Complement-mediated injury and protection of endothelium: lessons from atypical haemolytic uraemic syndrome.Immunobiology · 2012Review
- The role of antibodies in transplantation.Transplantation reviews (Orlando, Fla.) · 2009Review
- Mechanisms of complement activation, C4d deposition, and their contribution to the pathogenesis of antibody-mediated rejection.Transplantation reviews (Orlando, Fla.) · 2009Article
- Article
- Review
- Constitutive repression of interleukin-1alpha in endothelial cells.Circulation research · 2008Article
- Accommodation in organ transplantation.Current opinion in organ transplantation · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The barrier function of blood vessels is though to be regulated at least in part by endothelium. This concept is supported by the dramatic loss of barrier function occurring in the hyperacute rejection of vascularized grafts mediated by anti-endothelial cell (EC) antibodies and complement. In this process, the endothelium is not destroyed but instead loses the ability to retain blood cells and plasma proteins within capillaries. The noncytotoxic mechanism that allows this change in EC function has been unknown. Here we report that within 10 to 20 min of exposure to human xenoreactive natural antibodies and complement, porcine EC undergo alterations in cell shape and in the cytoskeleton that disrupt monolayer integrity and lead to formation of intercellular gaps. Gap formation is not associated with cell death but requires the complement complex C5b67. The gaps induced by anti-EC antibodies and complement are transient; gap closure requires formation of C5b-9 complexes on the cells and the rate of recovery depends on the release of cellular products into the medium. Preincubation of EC with dibutyryl cAMP (0.5 mM) prevents gap formation and disruption of the cytoskeleton caused by antibodies and complement. These results provide evidence that the integrity of endothelium is regulated by components of the complement system and suggest a mechanism that may explain the prominent loss of endothelial integrity seen in humoral immune responses.
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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.