By establishing a link between endogenous retroviruses, inflammation, and autoreactive T cells in lupus, research conducted by Akiko Iwasaki, PhD, has the potential to pave the way for new targeted therapies for this complex condition.
Akiko Iwasaki, PhD, Sterling Professor of Immunobiology and Molecular, Cellular, and Developmental Biology at Yale University and an investigator of the Howard Hughes Medical Institute, has been granted the 2023 Dr. William E. Paul Distinguished Innovator Award by the Lupus Research Alliance (LRA). Iwasaki and her team will use the prize to evaluate the immune response to increased endogenous retrovirus (ERV) levels as a trigger of autoimmunity in systemic lupus erythematosus (SLE).
ERVs, comprising about 8% of the human genome, are remnants of past viral infections in our ancestors. In individuals with SLE, there is an elevated production of inflammatory molecules called type I interferons, but the cause of this increase is not well understood. Iwasaki's recent findings suggest that ERVs become active and drive the heightened production of type I interferons.
In lupus, autoreactive T cells, which are part of the immune system's defense, can mistakenly target the body's own cells. This can lead to the activation of B cells, resulting in the production of autoantibodies that recognize the body's organs and tissues as foreign. Iwasaki and her team will measure the levels of ERVs and identify autoreactive T cells that target ERVs in individuals with cutaneous lupus, a form of lupus affecting the skin.
By establishing a link between ERVs, inflammation, and autoreactive T cells in lupus, Iwasaki's research has the potential to pave the way for new targeted therapies for this complex condition.
“I am honored and delighted to receive the LRA Distinguished Innovator Award!” Iwasaki said. “Lupus is an autoimmune disease, which means that our immune system attacks our own cells by mistake. Exactly what is being targeted by the immune system still remains a mystery. We hypothesize that immune reaction to viruses that live inside of our cells may be the culprit. We are developing the right tools to be able to probe this link, thanks to the support of LRA.”