ArticleClinical immunology (Orlando, Fla.)2012
Development of IgA nephropathy-like glomerulonephritis associated with Wiskott-Aldrich syndrome protein deficiency.
Article in Clinical immunology (Orlando, Fla.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 19 citations in OpenAlex.
- Exacerbated experimental arthritis in Wiskott-Aldrich syndrome protein deficiency: modulatory role of regulatory B cells.European journal of immunology · 2014Trial
- Wiskott-Aldrich syndrome and X-linked thrombocytopenia: a review of the clinical and immunological spectrum with a case presentation highlighting glomerulonephritis.Frontiers in pediatrics · 2026Review
- How I treat Wiskott-Aldrich syndrome.Blood · 2025Review
- A first-in-class Wiskott-Aldrich syndrome protein activator with antitumor activity in hematologic cancers.Haematologica · 2024Article
- A gain-of-function variant in the Wiskott-Aldrich syndrome gene is associated with a MYH9-related disease-like syndrome.Blood advances · 2022Article
- How I manage patients with Wiskott Aldrich syndrome.British journal of haematology · 2019Review
- Article
- Immune Complex-Mediated Glomerulonephritis in a Patient with Wiskott-Aldrich Syndrome.Journal of clinical immunology · 2016Article
- Unbalanced Immune System: Immunodeficiencies and Autoimmunity.Frontiers in pediatrics · 2016Review
- The clinical features of autoimmunity in 53 patients with Wiskott-Aldrich syndrome in China: a single-center study.European journal of pediatrics · 2015Article
- Age-Dependent Defects of Regulatory B Cells in Wiskott-Aldrich Syndrome Gene Knockout Mice.PloS one · 2015Article
- Allogeneic bone marrow transplantation appears to ameliorate IgA nephropathy in a patient with X-linked thrombocytopenia.Journal of clinical immunology · 2014Article
- Wiskott-Aldrich syndrome with IgA nephropathy: a case report and literature review.International urology and nephrology · 2013Review
- Wiskott-Aldrich syndrome protein-mediated actin dynamics control type-I interferon production in plasmacytoid dendritic cells.The Journal of experimental medicine · 2013Article
- Aberrant glycosylation of IgA in Wiskott-Aldrich syndrome and X-linked thrombocytopenia.The Journal of allergy and clinical immunology · 2013Article
- Autoimmunity in wiskott-Aldrich syndrome: an unsolved enigma.Frontiers in immunology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Wiskott-Aldrich syndrome (WAS) is a rare X-linked disorder caused by mutations in the WAS gene. Glomerulonephritis is a frequent complication, however, histopathological data from affected patients is scarce because the thrombocytopenia that affects most patients is a contraindication to renal biopsies. We found that WASp-deficient mice develop proliferative glomerulonephritis reminiscent of human IgA nephropathy (IgAN). We examined whether increased aberrant IgA production is associated with the development of glomerulonephritis in WASp-deficient mice. Serum IgA and IgA production by splenic B cells was increased in WASp-deficient mice compared to wild-type (WT) mice. A lectin-binding study revealed a reduced ratio of sialylated and galactosylated IgA in the sera from old WASp-deficient mice. Circulating IgA-containing immune complexes showed significantly higher titers in WASp-deficient mice compared to WT mice. These results indicate that the increased IgA production and aberrant glycosylation of IgA may be critically involved in the pathogenesis of glomerulonephritis in WAS.
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.