ArticleItalian journal of pediatrics2012
Interleukin 12 receptor deficiency in a child with recurrent bronchopneumonia and very high IgE levels.
Article in Italian journal of pediatrics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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, 8 citations in OpenAlex.
- Monocyte-regulated interleukin 12 production drives clearance of Staphylococcus aureus.PLoS pathogens · 2024Article
- [Changes in lymphocyte subsets in infants with common lower respiratory tract infectious diseases].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
- Regulation of Natural Killer Cell Function by STAT3.Frontiers in immunology · 2016Review
- The R156H variation in IL-12Rβ1 is not a mutation.Italian journal of pediatrics · 2013Article
- High immunoglobulin E level is associated with increased readmission in children with bronchopneumonia.Therapeutic advances in respiratory diseaseArticle
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9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-12 (IL-12) is involved in cellular immune responses against intracellular pathogens by promoting the generation of T naive in T helper 1 (Th1) cells and by increasing interferon-gamma (IFN-gamma) production from T and natural killer (NK) cells. A defective induction of a Th1 response may lead to a higher risk of infections, and, in particular, infections due to typical and atypical Mycobacteria. We report on the case of a girl with suffering from recurrent bronchopneumonia associated with very high serum IgE levels, who exhibited a profound impairment of the Th1 generation associated with a novel mutation in the exon 5 of the IL-12R β1 gene (R156H). Our data suggest that in children with severe and recurrent infections, even in the absence of a mycobacterial infection, functional and/or genetic alterations of the molecular mechanisms governing Th1/Th2 homeostasis might be responsible for an atypical immunodeficiency and, therefore, should be investigated in these patients.
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