ReviewClinical microbiology reviews2011
Infectious diseases in patients with IRAK-4, MyD88, NEMO, or IκBα deficiency.
Review in Clinical microbiology reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 191 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
191 citing papers in PubMed, 382 citations in OpenAlex.
- IRAK4 degrader in hidradenitis suppurativa and atopic dermatitis: a phase 1 trial.Nature medicine · 2023Trial
- IRAK-4 and MyD88 deficiencies impair IgM responses against T-independent bacterial antigens.Blood · 2014Trial
- TLR-mediated inflammatory responses to Streptococcus pneumoniae are highly dependent on surface expression of bacterial lipoproteins.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- When less is more: loss of IRAK2 signalling promotes inflammation.Nature reviews. Rheumatology · 2026Article
- Fungal Infections in Disorders of Inborn Errors of Immunity.Clinical reviews in allergy & immunology · 2026Review
- Human inborn errors of the alternative NF-κB pathway.Journal of human immunity · 2026Review
- Mendelian susceptibility to mycobacterial disease: IFN-γ-driven immunity collapse underlies heterogeneous infections.Frontiers in immunology · 2026Review
- The role of soluble toll-like receptor-2 and 4 in children with pneumonia: a combined analysis of saliva and serum samples.Frontiers in immunology · 2026Article
- Review
- To generate functional anti-protease-activated receptor-4 (PAR4), a G protein-coupled receptor, antibodies through PAR4-mRNA-LNP immunization.NPJ vaccines · 2025Article
- Regulation of toll-like receptor signaling pathways in age-related eye disease: from mechanisms to targeted therapeutics.Inflammopharmacology · 2025Review
- Role for IRAK-4 and p38 in Neutrophil Signaling in Response to Bacterial Lipoproteins from Staphylococcus aureus.Inflammation · 2025Article
- Pathological IgE Production in Inborn Errors of Immunity and Beyond.Immunological reviews · 2025Review
- Dynamics of antimicrobial proteins' expression and their bactericidal activity in mouse milk.ImmunoHorizons · 2025Article
- Bidirectional Communication Between the Innate and Adaptive Immune Systems.Annual review of immunology · 2025Review
- Evaluation of Inborn Errors of Immunity Among Patients with Opportunistic Pulmonary Infection.Clinics in chest medicine · 2025Review
- The monogenic landscape of human infectious diseases.The Journal of allergy and clinical immunology · 2025Review
- A 5-transcript signature for discriminating viral and bacterial etiology in pediatric pneumonia.iScience · 2025Article
- Mechanisms conferring multi-layered protection against intestinal Salmonella Typhimurium infection.FEMS microbiology reviews · 2025Review
- Partial Loss of NEMO Function in a Female Carrier with No Incontinentia Pigmenti.Journal of clinical medicine · 2025Article
131 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Autosomal recessive IRAK-4 and MyD88 deficiencies predispose affected patients to recurrent invasive pyogenic bacterial infection. Both defects result in the selective impairment of cellular responses to Toll-like receptors (TLRs) other than TLR3 and of cellular responses to most interleukin-1 receptors (IL-1Rs), including IL-1R, IL-18R, and IL-33R. Hypomorphic mutations in the X-linked NEMO gene and hypermorphic mutations in the autosomal IKBA gene cause X-linked recessive and autosomal dominant anhidrotic ectodermal dysplasia with immunodeficiency (EDA-ID) syndromes. Both of these defects impair NF-κB-mediated cellular responses to multiple receptors, including TLRs, IL-1Rs, and tumor necrosis factor receptors (TNF-Rs). They therefore confer a much broader predisposition to infections than that for IRAK-4 and MyD88 deficiencies. These disorders were initially thought to be rare but have now been diagnosed in over 170 patients worldwide. We review here the infectious diseases affecting patients with inborn errors of NF-κB-dependent TLR and IL-1R immunity.
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.