Interferon Regulation Could Reduce Severity of Lyme Disease Arthritis

The University of Utah Health website has reported news from the university’s Division of Microbiology and Immunology and their recent discovery of a new genetic pathway that might help to uncover why some patients develop more severe cases of Lyme disease arthritis.

Previous studies identified the association between severe Lyme arthritis and an elevated presence of interferon, which is an important regulator of the autoimmune response. However, due to its important role in regulating the immune system, inhibiting its activity would leave patients too susceptible to viral infections. To work around this issue, the U of U Health researchers took a deeper look at the genetic pathways that are involved in the production of interferon.

Their study of mouse cells revealed that Borrelia burgdorferi, the bacteria that causes Lyme disease, uses the p19ARF protein of the host to aid in interferon production. They also discovered that the p19ARF pathway is more active in the study segments that developed more severe Lyme arthritis.

Based on prior studies, the researchers were aware that variations in the severity of Lyme arthritis are caused by genetics of the bacteria while these new findings highlight the significance of genetic variations of the hosts.

The researchers tested the theory by reducing p19ARF genetic pathway activity in one set of laboratory mice while inducing elevated levels in a different set. Results showed that the specimens with elevated p19ARF genetic activity developed more severe Lyme arthritis symptoms.

The discovery of this genetic pathway offers valuable insights into how interferon regulation may affect the onset and advancement of Lyme as well as other diseases linked to heightened interferon levels.

Read the write-up on the University of Utah Health website.

Read the study published in PLOS Pathogens.