ArticleNature immunology2014
A narrow repertoire of transcriptional modules responsive to pyogenic bacteria is impaired in patients carrying loss-of-function mutations in MYD88 or IRAK4.
Article in Nature immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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48 citing papers in PubMed, 81 citations in OpenAlex.
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- Impact of MyD88 Deficiency on Innate Immune Function in COVID-19 Infection and Allotransplantation.Transplantation · 2023Article
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- Listeria Monocytogenes Meningoencephalitis Due to IRAK4 Deficiency.Journal of clinical immunology · 2021Article
- BloodGen3Module: blood transcriptional module repertoire analysis and visualization using R.Bioinformatics (Oxford, England) · 2021Article
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19 authors at 5 institutions in 2 countries.
Funding
Abstract
Loss of function of the kinase IRAK4 or the adaptor MyD88 in humans interrupts a pathway critical for pathogen sensing and ignition of inflammation. However, patients with loss-of-function mutations in the genes encoding these factors are, unexpectedly, susceptible to only a limited range of pathogens. We employed a systems approach to investigate transcriptome responses following in vitro exposure of patients' blood to agonists of Toll-like receptors (TLRs) and receptors for interleukin 1 (IL-1Rs) and to whole pathogens. Responses to purified agonists were globally abolished, but variable residual responses were present following exposure to whole pathogens. Further delineation of the latter responses identified a narrow repertoire of transcriptional programs affected by loss of MyD88 function or IRAK4 function. Our work introduces the use of a systems approach for the global assessment of innate immune responses and the characterization of human primary immunodeficiencies.
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