Until now, scientists believed this autoimmune response occurred because viral proteins mimicked the body’s own proteins, confusing the immune system into attacking both. The Garvan team revealed that this is not the case—rather, the critical trigger is mutations in “rogue clone” B cells.

“This discovery fundamentally changes our understanding of how infections can cause autoimmune conditions,” says Professor Chris Goodnow, Head of the Immunogenomics Lab at Garvan and the study’s co-senior author.

“By pinpointing these rogue clones, we can better understand how to target them, which is a potentially transformative approach to treating autoimmune disease in patients.”