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Lupus Biomarker Testing Could Help Identify Patients That Need Early and Aggressive Treatment

By LabMedica International staff writers
Posted on 31 Mar 2023
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Image: Researchers have identified the origin of subset of autoantibodies that worsen lupus (Photo courtesy of Pexels)
Image: Researchers have identified the origin of subset of autoantibodies that worsen lupus (Photo courtesy of Pexels)

Systemic lupus erythematosus (SLE) is an autoimmune disease that occurs when the body's antibodies, which usually protect against infections, attack healthy cells and proteins. These autoantibodies can cause inflammation and harm to various organ systems. Now, scientists researching the origins of SLE and the reasons why some patients have more severe symptoms than others have discovered a type of autoantibody that could worsen the disease and identified how these autoantibodies are formed. These findings may have implications for lupus biomarker testing and aid in the early detection and aggressive treatment of patients.

Before, it was unclear to researchers why the severity of SLE varied so greatly among patients who possess anti-DNA antibodies, which attack DNA. Investigators at Johns Hopkins Medicine (Baltimore, MD, USA) have discovered that a specific subset of these antibodies attacks DNase1L3, a critical enzyme in the body. Anti-DNA antibodies are a distinguishing feature of SLE patients, but not all such antibodies cause the disease, and their root cause is still unknown. To uncover the reasons behind the variation in SLE severity among patients with anti-DNA antibodies, the Johns Hopkins researchers looked at a different antibody that targets the enzyme DNase1L3. This enzyme plays a crucial role in clearing DNA from dead cells, and when it is blocked by antibodies, inflammation occurs due to the accumulation of DNA in the body.

In studying these antibodies, the researchers found that a subset of anti-DNase1L3 antibodies also targeted DNA in patients with severe SLE. To investigate the relationship between anti-DNase1L3 antibodies and severe SLE, the researchers analyzed blood and serum samples from 158 SLE patients and 62 non-lupus individuals. The results showed that high levels of illness were associated with antibodies that targeted both DNase1L3 and DNA, but only when both types of antibodies were present in patients, not just one class of antibody.

The researchers then went on to investigate the function and origin of these antibodies using molecular analysis. The results of the analysis were surprising as it revealed that the antibodies previously believed to target either DNA or DNase1L3 were actually a single antibody that could attack both molecules. The researchers suggest that this unique type of antibody could explain the variation in SLE severity among patients and why those who test positive for only one antibody may not develop severe SLE. The findings also challenge the current belief that DNA causes the formation of anti-DNA antibodies. Instead, the researchers propose that a subset of anti-DNA antibodies originates from anti-DNase1L3 antibodies, and that they acquire the ability to attack DNA through antibody mutations.

“Our findings provide a simple explanation for the differences of anti-DNA antibodies in SLE by demonstrating that some of these autoantibodies have multiple functions,” said corresponding author Felipe Andrade, M.D., Ph.D., an associate professor of medicine in the Division of Rheumatology at the Johns Hopkins University School of Medicine. “We hope these findings will improve ways of identifying patients with severe lupus and also help doctors choose appropriate treatments. This research may help uncover underlying mechanisms of lupus and why it affects patients differently.”

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Johns Hopkins Medicine

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