Their theory: A form of a gene that raises risk of lupus has a plus side - rendering the carrier more resistant to malaria.

That means the gene would be useful, and selected for, in areas of the world where malaria is rife. In those places, the downside of increased lupus risk would be far outweighed by the added protection against malaria.

And - like a fossil - the gene variant would persist in the DNA of people whose ancestors came from malarial regions, even when those people don't live with the threat of malaria.

The study, conducted by a team of British researchers, was published in the journal Proceedings of the National Academy of Sciences. It found higher rates of the gene variant in Hong Kong patients with lupus compared with matched controls - and it found lower rates of the gene variant in children in Kenya who had gotten malaria compared with the general population there.

The gene in this case (known as Fc gamma RIIB) is a receptor involved in the immune response, and so the finding makes sense - a ramped up immune system would help fight infection but could also raise the risk for autoimmune conditions.

It's a similar story to that seen with the gene for sickle cell disease. This gene protects against malaria, but when a person has two copies of it, it causes the sickle-cell blood disease. Rates of the mutations causing sickle cell disease remain higher in African Americans today.

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