Genetics may explain why infections can trigger rheumatoid arthritis

Genetics could explain why different environmental exposures can trigger the onset of different forms of rheumatoid arthritis, says an international study published in the American Journal of Human Genetics.

The findings could have important implications for the way that rheumatoid arthritis is diagnosed and treated.

Rheumatoid arthritis is an inflammatory form of arthritis, affecting almost 400,000 people in the UK, which causes painful, swollen joints, and in severe cases, considerable disability. It is known to have strong genetic and environmental components.

It was already known that some people with rheumatoid arthritis test positive for autoantibodies, whilst about 30% remain sero-negative. In this study, the researchers have better defined the genetic distinction between these two disease subtypes: sero-positive and sero-negative rheumatoid arthritis.

The team has established that different genetic variants of a protein that plays a vital role in how the body’s immune system fights infection are associated with the two forms of rheumatoid arthritis. This provides clues to the theory that exposure to different infectious agents, such as bacteria or viruses, trigger the different forms of rheumatoid arthritis in susceptible individuals.  Sero-negative rheumatoid is less well understood than sero-positive, and people who have this type of arthritis can be misdiagnosed, leading to inappropriate treatment.

“Now that we have established a genetic basis for these two types of rheumatoid arthritis, we hope it will lead to patients receiving a swifter, accurate diagnosis and more appropriate, targeted treatment,” says Prof Jane Worthington from the genetics and genomics centre in Manchester, which was involved in the work. “These findings have opened the door to a better understanding of sero-negative rheumatoid arthritis.”