Trial reportJournal of immunology (Baltimore, Md. : 1950)2014
The combined role of galactose-deficient IgA1 and streptococcal IgA-binding M Protein in inducing IL-6 and C3 secretion from human mesangial cells: implications for IgA nephropathy.
Trial report in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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
26 citing papers in PubMed, 57 citations in OpenAlex.
- Intrinsic renal cells induce lymphocytosis of Th22 cells from IgA nephropathy patients through B7-CTLA-4 and CCL-CCR pathways.Molecular and cellular biochemistry · 2018Trial
- IgA nephropathy new therapies: from data in adults to application in children.Pediatric nephrology (Berlin, Germany) · 2026Review
- Pathogenic Immunoglobulin A-Producing Cells in Immunoglobulin A Nephropathy.Journal of clinical medicine · 2024Review
- Investigating Vitamin D-Binding Protein's Role in Childhood Health and Development.International journal of molecular sciences · 2024Review
- Small protein blockers of human IL-6 receptor alpha inhibit proliferation and migration of cancer cells.Cell communication and signaling : CCS · 2024Article
- Sparsentan ameliorates glomerular hypercellularity and inflammatory-gene networks induced by IgA1-IgG immune complexes in a mouse model of IgA nephropathy.American journal of physiology. Renal physiology · 2024Article
- Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy.Frontiers in medicine · 2023Review
- Article
- Cytokines and Production of AberrantlyJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Review
- Gut-kidney axis in IgA nephropathy: Role on mesangial cell metabolism and inflammation.Frontiers in cell and developmental biology · 2022Review
- Autoimmune-mediated renal disease and hypertension.Clinical science (London, England : 1979) · 2021Review
- New therapeutic perspectives for IgA nephropathy in children.Pediatric nephrology (Berlin, Germany) · 2021Review
- Renal diseases and the role of complement: Linking complement to immune effector pathways and therapeutics.Advances in immunology · 2021Review
- An Update on Targeted Treatment of IgA Nephropathy: An Autoimmune Perspective.Frontiers in pharmacology · 2021Review
- Emerging Modes of Treatment of IgA Nephropathy.International journal of molecular sciences · 2020Review
- The Role of Immune Modulation in Pathogenesis of IgA Nephropathy.Frontiers in medicine · 2020Review
- Mesangial Cells Exhibit Features of Antigen-Presenting Cells and Activate CD4+ T Cell Responses.Journal of immunology research · 2019Article
- C4d deposits in IgA nephropathy: where does complement activation come from?Pediatric nephrology (Berlin, Germany) · 2017Article
- Biomarkers and targeted new therapies for IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2017Review
- The risk of IgA nephropathy and glomerular disease in patients with psoriasis: a population-based cohort study.The British journal of dermatology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
IgA nephropathy (IgAN) is characterized by mesangial cell proliferation and extracellular matrix expansion associated with immune deposits consisting of galactose-deficient polymeric IgA1 and C3. We have previously shown that IgA-binding regions of streptococcal M proteins colocalize with IgA in mesangial immune deposits in patients with IgAN. In the present study, the IgA-binding M4 protein from group A Streptococcus was found to bind to galactose-deficient polymeric IgA1 with higher affinity than to other forms of IgA1, as shown by surface plasmon resonance and solid-phase immunoassay. The M4 protein was demonstrated to bind to mesangial cells not via the IgA-binding region but rather via the C-terminal region, as demonstrated by flow cytometry. IgA1 enhanced binding of M4 to mesangial cells, but not vice versa. Costimulation of human mesangial cells with M4 and galactose-deficient polymeric IgA1 resulted in a significant increase in IL-6 secretion compared with each stimulant alone. Galactose-deficient polymeric IgA1 alone, but not M4, induced C3 secretion from the cells, and costimulation enhanced this effect. Additionally, costimulation enhanced mesangial cell proliferation compared with each stimulant alone. These results indicate that IgA-binding M4 protein binds preferentially to galactose-deficient polymeric IgA1 and that these proteins together induce excessive proinflammatory responses and proliferation of human mesangial cells. Thus, tissue deposition of streptococcal IgA-binding M proteins may contribute to the pathogenesis of IgAN.
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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.