ArticleJournal of clinical immunology2009
Cellular and molecular characterisation of the hyper immunoglobulin M syndrome associated with congenital rubella infection.
Article in Journal of clinical immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 17 citations in OpenAlex.
- Type 2 hyper-IgM syndrome with a rare variant of AICDA gene mutation in a young woman.BMJ case reports · 2023Article
- Hyper-IgM and acquired C1q complement deficiency in a patient withOxford medical case reports · 2023Article
- SARS-CoV-2 Omicron: Light at the End of the Long Pandemic Tunnel or Another False Dawn for Immunodeficient Patients?The journal of allergy and clinical immunology. In practice · 2022Article
- Identification of germinal centres in the lymph node of a patient with hyperimmunoglobulin M syndrome associated with congenital rubella.Journal of clinical immunology · 2014Article
- The clinical utility of molecular diagnostic testing for primary immune deficiency disorders: a case based review.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe hyper-immunoglobulin M syndrome (HIM) is a rare group of immune deficiency disorders characterised by normal or increased serum IgM with normal or reduced IgG, IgA and IgE. MATERIALS AND
methodsWe have undertaken detailed cellular and molecular studies in a 53-year-old man with HIM as a result of congenital rubella.
resultsNo mutations were detected in the CD40 ligand, activation-induced cytidine deaminase and uracil DNA glycosylase. His T-cell responses to lectins and antigens were normal. Flow cytometry confirmed the presence of CD40 ligand on activated T cells. Most CD40-dependent functions that were tested, including B-cell proliferation, isotype switching and production of memory B cells, were normal. CD40/IL4 dependent rescue from anti-IgM-induced apoptosis was impaired.
conclusionThe detection of cell-surface IgG but lack of serum IgG indicated that he may have an antibody secretion defect.
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Registered trials
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