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Genetics of SLE: does this explain susceptibility and severity across racial groups?

Research output: Contribution to journalArticlepeer-review

Original languageEnglish
Early online date30 Dec 2022
Accepted/In press12 Dec 2022
E-pub ahead of print30 Dec 2022

Bibliographical note

© The Author(s) 2022. Published by Oxford University Press on behalf of the British Society for Rheumatology.

King's Authors


The prevalence and severity of systemic lupus erythematosus (SLE) have been found to vary across populations of different ancestries. This review explores whether these differences can be explained by the genetic aetiology of the condition. Large genetic studies suggest that populations of different ancestry share the same risk loci but the individual risk alleles are more common in some, leading to a higher prevalence, severity, and earlier onset of the condition. Despite many of the loci being shared across populations, some have been found to be ancestry-specific and these are hypothesised to have undergone differential selective pressure in recent human history. Additionally, the effectiveness of some of the drugs used in SLE has been found to vary across ancestries, which might affect the progression of the disease, but it is unclear whether these differences are pharmacogenetic. We concluded that to understand the full role of genetics in the risk, presentation and response to treatment of SLE, larger studies including individuals from a wider representation of ancestries will be required.

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