LRA funds research exploring the role of ancient viruses in lupus
Akiko Iwasaki honored with Dr. William E. Paul Distinguished Innovator Award
Scientist Akiko Iwasaki will receive the Dr. William E. Paul Distinguished Innovator Award (DIA) to investigate whether ancient viral DNA in our cells is a potential trigger for lupus.
The $1 million award from the Lupus Research Alliance (LRA) will fund a four-year research project to investigate whether the immune system’s reaction to viral elements in our DNA, called endogenous retroviruses, is a potential trigger for the disease. About 8% of the human genome is composed of endogeneous retroviral genetic material, a genetic legacy from viruses that infected our human ancestors millions of years ago.
“I am honored and delighted to receive the LRA Distinguished Innovator Award! With this award, we will probe the link between the immune system reacting to viruses within us as a possible trigger of lupus disease,” Iwasaki, PhD, Sterling professor of Immunobiology at the Yale School of Medicine, said in a press release. “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.”
The findings may not only advance scientists’ current knowledge on the causes of lupus, but also help develop new and effective targeted therapies for the condition.
“We are thrilled to award the 2023 DIA to Dr. Iwasaki, whose innovative work has the potential to advance our understanding of a previously undescribed pathway to lupus with future therapeutic potential,” said Teodora Staeva, PhD, LRA’s chief scientific officer.
Underlying reason for immune response poorly understood
The autoimmune response that characterizes lupus is driven by inflammatory T-cells and the production of self-reactive antibodies by B-cells. Moreover, type 1 interferon molecules, which are normally produced in response to infections, are elevated in many people with lupus. However, the underlying reasons for this enhanced immune response directed against the body’s own tissues remains poorly understood.
Recent data from Iwasaki’s lab suggest the activation of endogenous retroviruses may lead to an increase in type 1 interferons. Researchers now will now use samples from people with cutaneous lupus, a form of the disease that predominately affects the skin, to measure the levels of endogenous retroviruses, as well as identify and characterize the T-cells targeting these viral remnants.
The team also will conduct a series of experiments in a mouse model of cutaneous lupus to investigate how the enhanced activation of endogenous retroviruses in the skin drives inflammation and autoimmunity.