Cited by 153Tuberculosis Research and EpidemiologyImmune responses and vaccinationsGenetic Associations and Epidemiology

Interleukin‐10, Polymorphism in SLC11A1(formerly NRAMP1), and Susceptibility to Tuberculosis

Awomoyi, Agnes A., Marchant, Arnaud, Howson, Joanna M. M., McAdam, Keith P. W. J., Blackwell, Jenefer M., Newport, Melanie J.·2002·The Journal of Infectious Diseases

Abstract

Host genetic factors are major determinants of susceptibility to tuberculosis, and an understanding of the molecular basis of this observation has major implications for the development of novel therapies and vaccines. Slc11a1 (formerly Nramp1), the first murine infection susceptibility locus identified, regulates early innate responses to intracellular pathogens. Variation in the human homologue SLC11A1 is associated with and linked to tuberculosis in genetically different populations. In a case-control study of 329 tuberculosis case patients and 324 control subjects, the association between allele 2 of a functional SLC11A1 polymorphism and tuberculosis has been reproduced. This variant is associated with higher lipopolysaccharide-induced production of the macrophage-deactivating cytokine interleukin-10. Furthermore, monocytes from persons who develop tuberculosis innately produce more interleukin-10 than do monocytes from healthy control subjects. These data therefore confirm the importance of SLC11A1 in tuberculosis susceptibility in humans and suggest that SLC11A1 influences tuberculosis susceptibility by regulation of interleukin-10.

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Crossref · 10.1086/345920

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  • In both humans and mice, NRAMP1 function affects the balance between proinflammatory mediators such as TNF and IFN-γ and antiinflammatory mediators such as IL-10 towards adequate production of the former.

    “In both humans and mice, the function of NRAMP1 affects the balance between proinflammatory mediators such as TNF and IFN-γ and antiinflammatory ones such as IL-10 towards adequate production of the former (Awomoyi et al., 2002;Fritsche et al., 2003Fritsche et al., , 2008;;Kovarova et al., 2000).”

    From Iron in infection and immunity (2020) · cites this paper as Awomoyi et al., 2002

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Authors
Awomoyi, A. A., Marchant, A., Howson, J. M. M., McAdam, K. P. W. J., Blackwell, J. M., & Newport, M. J.
Affiliations
  • MRC Unit the Gambia (GM)
  • John Radcliffe Hospital (GB)
  • Addenbrooke's Hospital (GB)
Corresponding author
Awomoyi, Agnes A.
Venue
The Journal of Infectious Diseases
Published
2002-12-15
Volume
186
Issue
12
Pages
1808-1814
ISSN
  • 0022-1899 (ISSN-L)
  • 1537-6613
OpenAlex
W2171429463
Cited by
153
References
54
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2021: 2 · 2020: 4 · 2019: 5 · 2018: 4 · 2017: 7 · 2016: 4 · 2015: 5 · 2014: 8 · 2013: 11 · 2012: 9
FWCI
7.56
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Infectious Diseases (publishedVersion)
  • PubMed (publishedVersion)
  • UWA Profiles and Research Repository (UWA) (submittedVersion)
  • Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
  • Figshare (submittedVersion)
  • Sussex Research Online (University of Sussex) (submittedVersion)
Funders
  • Alexander and Margaret Stewart Trust
  • Wellcome Trust (065642)
  • Sir Halley Stewart Trust
  • Medical Research Council
Topics
  • Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
  • Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
Keywords
tuberculosis susceptibility, SLC11A1, NRAMP1, IL-10, genetic polymorphism, host genetic factors, monocytes, lipopolysaccharide, innate immunity, intracellular pathogens
MeSH terms
Natural Resistance-associated Macrophage Protein 1, Adult, Alleles, Gambia, Genotype, Humans, Immunity, Innate, Male, Middle Aged, Monocytes, Mycobacterium tuberculosis, Polymorphism, Genetic, Tuberculosis, Pulmonary, Case-Control Studies, Interleukin-10, Genetic Predisposition to Disease, Cation Transport Proteins

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