ArticleThe American journal of pathology1998
Modulation of endothelial cell function by normal polyspecific human intravenous immunoglobulins: a possible mechanism of action in vascular diseases.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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Who cites it
23 citing papers in PubMed, 81 citations in OpenAlex.
- Polyclonal breast milk-derived secretory IgA confers broad antiviral protection against multiple respiratory viruses.Science advances · 2026Article
- The Potential Role of Endothelial Cells in the Pathophysiology, Diagnosis, and Management of Acute Kawasaki Disease.CJC open · 2026Review
- The Effect on Quality of Life of Therapeutic Plasmapheresis and Intravenous Immunoglobulins on a Population of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients with Elevated β-Adrenergic and M3-Muscarinic Receptor Antibodies-A Pilot Study.Journal of clinical medicine · 2025Article
- Review
- Application of intravenous immunoglobulin (IVIG) to modulate inflammation in critical COVID-19 - A theoretical perspective.Medical hypotheses · 2021Article
- Merits and culprits of immunotherapies for neurological diseases in times of COVID-19.EBioMedicine · 2020Review
- Phenotypic and Transcriptomic Lymphocytes Changes in Allograft Recipients After Intravenous Immunoglobulin Therapy in Kidney Transplant Recipients.Frontiers in immunology · 2020Article
- Disruption of Endothelial Cell Homeostasis Plays a Key Role in the Early Pathogenesis of Coronary Artery Abnormalities in Kawasaki Disease.Scientific reports · 2017Article
- Therapeutic Potential of Intravenous Immunoglobulin in Acute Brain Injury.Frontiers in immunology · 2017Review
- Therapeutic effect of IVIG on inflammatory arthritis in mice is dependent on the Fc portion and independent of sialylation or basophils.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Bench-to-bedside review: Immunoglobulin therapy for sepsis - biological plausibility from a critical care perspective.Critical care (London, England) · 2012Review
- Immunoglobulin g (IgG) expression in human umbilical cord endothelial cells.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2011Article
- Kawasaki disease: aetiopathogenesis and therapeutic utility of intravenous immunoglobulin.Autoimmunity reviews · 2010Review
- Current proposed mechanisms of action of intravenous immunoglobulins in inflammatory neuropathies.Current neuropharmacology · 2009Article
- Involvement of innate and adaptive immunity in a murine model of coronary arteritis mimicking Kawasaki disease.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- VASCULAR INFLAMMATION AND ATHEROGENESIS ARE ACTIVATED VIA RECEPTORS FOR PAMPs AND SUPPRESSED BY REGULATORY T CELLS.Drug discovery today. Therapeutic strategies · 2008Article
- Kawasaki disease.Yonsei medical journal · 2006Review
- Basic principles of intravenous immunoglobulin (IVIg) treatment.Journal of neurology · 2006Review
- Effect of maternal anti-HPA-1a antibodies and polyclonal IVIG on the activation status of vascular endothelial cells.Clinical and experimental immunology · 2004Article
- Normal human IgG prevents endothelial cell activation induced by TNFalpha and oxidized low-density lipoprotein atherogenic stimuli.Clinical and experimental immunology · 2003Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intravenous immunoglobulin (IVIg) is increasingly used in the treatment of autoimmune and inflammatory diseases, including vasculitides and Kawasaki disease. However, the outcome of IVIg interaction with endothelial cells of the vascular bed is not clear as yet. We have investigated the effect of IVIg on the in vitro activation of human endothelial cells, as assessed by cell proliferation and reverse transcription-polymerase chain reaction-detected expression of mRNA coding for adhesion molecules (intercellular adhesion molecule-1 and vascular cellular adhesion molecule-1), chemokines (monocyte chemoattractant protein-1, macrophage colony-stimulating factor, and granulocyte-macrophage colony-stimulating factor), and proinflammatory cytokines (tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6). IVIg inhibited proliferation of endothelial cells in a time-dependent manner. This effect was dependent on both Fc and F(ab')2 fragments of the immunoglobulin molecule and was fully reversible. Tumor necrosis factor-alpha and interleukin-1beta also inhibited thymidine incorporation, but to a lesser degree. IVIg had no effect on basal levels of mRNA coding for the adhesion molecules, chemokines, and proinflammatory cytokines. IVIg fully down-regulated the expression induced by tumor necrosis factor-alpha or interleukin-1beta of mRNA coding for these molecules. Thus, blockade of cellular proliferation and of cytokine-induced expression of adhesion molecules, chemokines, and cytokines may explain the therapeutic effect of IVIg in vascular and inflammatory disorders.
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