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 and Newport, Melanie J (2002) Interleukin-10, polymorphism in SLC11A1 (formerly NRAMP1), and susceptibility to tuberculosis. Journal of Infectious Diseases, 186 (12). pp. 1808-1814. ISSN 0022-1899

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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.

Item Type: Article
Schools and Departments: Brighton and Sussex Medical School > Primary Care and Public Health
Brighton and Sussex Medical School > Global Health and Infection
Subjects: R Medicine > RC Internal medicine > RC0251 Constitutional diseases (General)
Depositing User: pam Thompson
Date Deposited: 08 May 2014 17:24
Last Modified: 21 Sep 2017 13:37
URI: http://sro.sussex.ac.uk/id/eprint/48399
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