ReviewAnnals of the New York Academy of Sciences2015
Toll-like receptor signaling in primary immune deficiencies.
Review in Annals of the New York Academy of Sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 81 citations in OpenAlex.
- Endosome restricted human TLR1 polymorphism highlights a role for MyD88 in Pam3CSK4 detection.PloS one · 2026Article
- Gastroenterological disorders in inborn errors of immunity. Part 2B. Overview of selected diseases.Przeglad gastroenterologiczny · 2026Review
- Review
- Pulmonary Manifestations of Inborn Errors of Immunity: Diagnostic and Therapeutic Insights.Life (Basel, Switzerland) · 2025Review
- The potential impacts of human genetics on virus emergence.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Langerhans Cell Modulation in Atopic Dermatitis Is TLR2/SOCS1-Dependent and JAK Inhibitor-Sensitive.Allergy · 2025Article
- Mucosal Immunity: Lessons from the Lower Respiratory and Small Intestinal Epithelia.Biomedicines · 2025Review
- Label-free biosensor assay decodes the dynamics of Toll-like receptor signaling.Nature communications · 2024Article
- Oral Diseases as a Manifestation of Inborn Errors of Immunity.Journal of clinical medicine · 2024Review
- Immunoglobulin class-switch recombination: Mechanism, regulation, and related diseases.MedComm · 2024Review
- Article
- Intrinsic B cell TLR-BCR linked coengagement induces class-switched, hypermutated, neutralizing antibody responses in absence of T cells.Science advances · 2023Article
- Correlations between preclinical BJAB assay ranking of antisense drugs and clinical trial adverse events.Clinical and translational science · 2023Article
- Trained immunity: A "new" weapon in the fight against infectious diseases.Frontiers in immunology · 2023Review
- Clinical Implication of Toll-Like Receptors (TLR2 and TLR4) Polymorphisms in Adult Patients with Acute B-cell Lymphoblastic Leukemia.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Review
- Effective, safe, and sustained correction of murine XLA using a UCOE-BTK promoter-based lentiviral vector.Molecular therapy. Methods & clinical development · 2021Article
- Revealing the Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Chromosome-Scale Genome of Masked Palm Civet (Frontiers in genetics · 2021Article
- The microbiome and its impact on food allergy and atopic dermatitis in children.Postepy dermatologii i alergologii · 2020Review
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 1 institution in 1 country.
Funding
Abstract
Toll-like receptors (TLRs) recognize common microbial or host-derived macromolecules and have important roles in early activation of the immune system. Patients with primary immune deficiencies (PIDs) affecting TLR signaling can elucidate the importance of these proteins to the human immune system. Defects in interleukin-1 receptor-associated kinase-4 and myeloid differentiation factor 88 (MyD88) lead to susceptibility to infections with bacteria, while mutations in nuclear factor-κB essential modulator (NEMO) and other downstream mediators generally induce broader susceptibility to bacteria, viruses, and fungi. In contrast, TLR3 signaling defects are specific for susceptibility to herpes simplex virus type 1 encephalitis. Other PIDs induce functional alterations of TLR signaling pathways, such as common variable immunodeficiency in which plasmacytoid dendritic cell defects enhance defective responses of B cells to shared TLR agonists. Dampening of TLR responses is seen for TLRs 2 and 4 in chronic granulomatous disease (CGD) and X-linked agammaglobulinemia (XLA). Enhanced TLR responses, meanwhile, are seen for TLRs 5 and 9 in CGD, TLRs 4, 7/8, and 9 in XLA, TLRs 2 and 4 in hyper IgE syndrome, and for most TLRs in adenosine deaminase deficiency.
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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.