ArticleProceedings of the National Academy of Sciences of the United States of America2017
Inherited human IRAK-1 deficiency selectively impairs TLR signaling in fibroblasts.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 56 citations in OpenAlex.
- Enteric nervous system in microbiota-associated gut inflammation.Frontiers in immunology · 2026Review
- Unraveling the role of IRAK1 in autoimmune rheumatic diseases: beyond genetic associations.Molecular biology reports · 2025Article
- Contribution of Interleukin-1 Receptor-Associated Kinase 1 Gene Polymorphism to Systemic Lupus Erythematosus in Chinese Patients.Journal of inflammation research · 2025Article
- Selective targeting of IRAK1 attenuates low molecular weight hyaluronic acid-induced stemness and non-canonical STAT3 activation in epithelial ovarian cancer.Cell death & disease · 2024Article
- Bacterial surface lipoproteins mediate epithelial microinvasion byInfection and immunity · 2024Article
- Regulation of innate immune signaling by IRAK proteins.Frontiers in immunology · 2023Review
- Nonhematopoietic IRAK1 drives arthritis via neutrophil chemoattractants.JCI insight · 2022Article
- SMRT and NCoR1 fine-tune inflammatory versus tolerogenic balance in dendritic cells by differentially regulating STAT3 signaling.Frontiers in immunology · 2022Article
- IRAK4 Deficiency Presenting with Anti-NMDAR Encephalitis and HHV6 Reactivation.Journal of clinical immunology · 2021Article
- Suppression of monosodium urate crystal-induced inflammation by inhibiting TGF-β-activated kinase 1-dependent signaling: role of the ubiquitin proteasome system.Cellular & molecular immunology · 2021Article
- Kinase inhibition in autoimmunity and inflammation.Nature reviews. Drug discovery · 2021Review
- Escape from X chromosome inactivation and female bias of autoimmune diseases.Molecular medicine (Cambridge, Mass.) · 2020Review
- Intestinal Bacteria Maintain Adult Enteric Nervous System and Nitrergic Neurons via Toll-like Receptor 2-induced Neurogenesis in Mice.Gastroenterology · 2020Article
- The genetic basis of pneumococcal and staphylococcal infections: inborn errors of human TLR and IL-1R immunity.Human genetics · 2020Review
- Susceptibility to infection in early life: a growing role for human genetics.Human genetics · 2020Review
- T Cell Impairment Is Predictive for a Severe Clinical Course in NEMO Deficiency.Journal of clinical immunology · 2020Article
- The role of microbiota in the development of colorectal cancer.International journal of cancer · 2019Review
- Lessons learned from the study of human inborn errors of innate immunity.The Journal of allergy and clinical immunology · 2019Review
- TLR4 signaling improves PD-1 blockade therapy during chronic viral infection.PLoS pathogens · 2019Article
- Human Toll-like Receptor 8 (TLR8) Is an Important Sensor of Pyogenic Bacteria, and Is Attenuated by Cell Surface TLR Signaling.Frontiers in immunology · 2019Article
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Authors and funding
26 authors at 9 institutions in 4 countries.
Funding
Abstract
Most members of the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) families transduce signals via a canonical pathway involving the MyD88 adapter and the interleukin-1 receptor-associated kinase (IRAK) complex. This complex contains four molecules, including at least two (IRAK-1 and IRAK-4) active kinases. In mice and humans, deficiencies of IRAK-4 or MyD88 abolish most TLR (except for TLR3 and some TLR4) and IL-1R signaling in both leukocytes and fibroblasts. TLR and IL-1R responses are weak but not abolished in mice lacking IRAK-1, whereas the role of IRAK-1 in humans remains unclear. We describe here a boy with X-linked MECP2 deficiency-related syndrome due to a large de novo Xq28 chromosomal deletion encompassing both MECP2 and IRAK1 Like many boys with MECP2 null mutations, this child died very early, at the age of 7 mo. Unlike most IRAK-4- or MyD88-deficient patients, he did not suffer from invasive bacterial diseases during his short life. The IRAK-1 protein was completely absent from the patient's fibroblasts, which responded very poorly to all TLR2/6 (PAM
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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.