Observational studyTuberculosis (Edinburgh, Scotland)2017
The SIGLEC14 null allele is associated with Mycobacterium tuberculosis- and BCG-induced clinical and immunologic outcomes.
Observational study in Tuberculosis (Edinburgh, Scotland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- An integrative genomics approach identifies KDM4 as a modulator of trained immunity.European journal of immunology · 2022Pooled it
- Protective Role of The SIGLEC14 Null Allele Against Type 2 Diabetes Mellitus: Evidence From an Egyptian Case-Control Study.Molecular biology reports · 2026Article
- Article
- Article
- Discovery, classification, evolution and diversity of Siglecs.Molecular aspects of medicine · 2023Review
- Metabolites enhance innate resistance to human Mycobacterium tuberculosis infection.JCI insight · 2022Article
- Human M1 macrophages express unique innate immune response genes after mycobacterial infection to defend against tuberculosis.Communications biology · 2022Article
- Common determinants of severe Covid-19 infection are explicable by SARS-CoV-2 secreted glycoprotein interaction with the CD33-related Siglecs, Siglec-3 and Siglec-5/14.Medical hypotheses · 2020Article
- Genetics and evolution of tuberculosis pathogenesis: New perspectives and approaches.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2020Review
- Evaluation of CD33 as a genetic risk factor for Alzheimer's disease.Acta neuropathologica · 2019Review
- Possible Influences of Endogenous and Exogenous Ligands on the Evolution of Human Siglecs.Frontiers in immunology · 2018Review
- Article
- Heterogeneity in tuberculosis.Nature reviews. Immunology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 8 institutions in 6 countries.
Funding
Abstract
Humans exposed to Mycobacterium tuberculosis (Mtb) have variable susceptibility to tuberculosis (TB) and its outcomes. Siglec-5 and Siglec-14 are members of the sialic-acid binding lectin family that regulate immune responses to pathogens through inhibitory (Siglec-5) and activating (Siglec-14) domains. The SIGLEC14 coding sequence is deleted in a high proportion of individuals, placing a SIGLEC5-like gene under the expression of the SIGLEC14 promoter (the SIGLEC14 null allele) and causing expression of a Siglec-5 like protein in monocytes and macrophages. We hypothesized that the SIGLEC14 null allele was associated with Mtb replication in monocytes, T-cell responses to the BCG vaccine, and clinical susceptibility to TB. The SIGLEC14 null allele was associated with protection from TB meningitis in Vietnamese adults but not with pediatric TB in South Africa. The null allele was associated with increased IL-2 and IL-17 production following ex-vivo BCG stimulation of blood from 10 week-old South African infants vaccinated with BCG at birth. Mtb replication was increased in THP-1 cells overexpressing either Siglec-5 or Siglec-14 relative to controls. To our knowledge, this is the first study to demonstrate an association between SIGLEC expression and clinical TB, Mtb replication, or BCG-specific T-cell cytokines.
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.