ArticleScientific reports2014
Intravenous immunoglobulin-induced IL-33 is insufficient to mediate basophil expansion in autoimmune patients.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- A Phase I/IIa Trial of Intravenous Immunoglobulin Following Portoenterostomy in Biliary Atresia.Journal of pediatric gastroenterology and nutrition · 2019Trial
- The role of antibody glycosylation in autoimmune and alloimmune kidney diseases.Nature reviews. Nephrology · 2024Review
- An overview of some potential immunotherapeutic options against COVID-19.International immunopharmacology · 2021Review
- Immunoglobulin G Glycosylation Changes in Aging and Other Inflammatory Conditions.Experientia supplementum (2012) · 2021Article
- Sialylated immunoglobulin G: a promising diagnostic and therapeutic strategy for autoimmune diseases.Theranostics · 2021Review
- Convalescent plasma in Covid-19: Possible mechanisms of action.Autoimmunity reviews · 2020Review
- Natural Antibodies: from First-Line Defense Against Pathogens to Perpetual Immune Homeostasis.Clinical reviews in allergy & immunology · 2020Review
- Structural insights into the mechanisms and specificities of IgG-active endoglycosidases.Glycobiology · 2020Review
- Therapeutic normal IgG intravenous immunoglobulin activates Wnt-β-catenin pathway in dendritic cells.Communications biology · 2020Article
- Intravenous immunoglobulin mediates anti-inflammatory effects in peripheral blood mononuclear cells by inducing autophagy.Cell death & disease · 2020Article
- Differential antibody glycosylation in autoimmunity: sweet biomarker or modulator of disease activity?Nature reviews. Rheumatology · 2017Review
- IVIG regulates the survival of human but not mouse neutrophils.Scientific reports · 2017Article
- Regulatory T cell frequency, but not plasma IL-33 levels, represents potential immunological biomarker to predict clinical response to intravenous immunoglobulin therapy.Journal of neuroinflammation · 2017Article
- Predisposing factors, pathogenesis and therapeutic intervention of Kawasaki disease.Drug discovery today · 2016Review
- Immune recruitment or suppression by glycan engineering of endogenous and therapeutic antibodies.Biochimica et biophysica acta · 2016Review
- Article
- Heme oxygenase-1 is dispensable for the anti-inflammatory activity of intravenous immunoglobulin.Scientific reports · 2016Article
- Anti-inflammatory activity of intravenous immunoglobulins protects against West Nile virus encephalitis.The Journal of general virology · 2015Article
- Protection in antibody- and T cell-mediated autoimmune diseases by antiinflammatory IgG Fcs requires type II FcRs.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Differences in Anti-Inflammatory Actions of Intravenous Immunoglobulin between Mice and Men: More than Meets the Eye.Frontiers in immunology · 2015Review
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intravenous immunoglobulin (IVIg) is used in the therapy of various autoimmune and inflammatory diseases. Recent studies in experimental models propose that anti-inflammatory effects of IVIg are mainly mediated by α2,6-sialylated Fc fragments. These reports further suggest that α2,6-sialylated Fc fragments interact with DC-SIGN(+) cells to release IL-33 that subsequently expands IL-4-producing basophils. However, translational insights on these observations are lacking. Here we show that IVIg therapy in rheumatic patients leads to significant raise in plasma IL-33. However, IL-33 was not contributed by human DC-SIGN(+) dendritic cells and splenocytes. As IL-33 has been shown to expand basophils, we analyzed the proportion of circulating basophils in these patients following IVIg therapy. In contrast to mice data, IVIg therapy led to basophil expansion only in two patients who also showed increased plasma levels of IL-33. Importantly, the fold-changes in IL-33 and basophils were not correlated and we could hardly detect IL-4 in the plasma following IVIg therapy. Thus, our results indicate that IVIg-induced IL-33 is insufficient to mediate basophil expansion in autoimmune patients. Hence, IL-33 and basophil-mediated anti-inflammatory mechanism proposed for IVIg might not be pertinent in humans.
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