An engineered protein that can deactivate immune cells responsible for tissue damage in autoimmune diseases has been developed, according to a study published in the journal Cell. The research focused on type 1 diabetes, hepatitis, and multiple sclerosis, where T cells mistakenly attack the body’s own tissues.
The study, led by researchers from NYU Langone Health, the Chinese Academy of Sciences, and Zhejiang University, introduced an antibody designed to target two signaling complexes on T cells. This approach was shown to limit autoimmune tissue damage in mice models.
Jun Wang, PhD, assistant professor at NYU Grossman School of Medicine and co-senior author of the study stated: “Our findings reveal an intricate mechanism that enables a careful treatment approach to T cell–driven autoimmune diseases, which currently lack effective immunotherapies.”
The study highlights how T-cell receptors (TCRs) are activated by bits of bacteria or viruses but can also be triggered by the body’s proteins in autoimmune conditions. LAG-3 checkpoints work oppositely by suppressing T cell activity when turned on. Jasper Du, a medical student involved in the research noted: “We discovered that…the T cell receptor gets particularly close to LAG-3,” which is key for reducing T cell activity.
The researchers created a bispecific antibody named BiTS (LAG-3/TCR Bispecific T cell Silencer), which showed effectiveness in reducing inflammatory damage and lessening disease symptoms in mouse models with autoimmune diseases.
Jia You, another researcher involved said: “Our study advances our understanding of LAG-3 biology and may foster more proximity-based…therapeutic designs like BiTS as immunotherapy for other human diseases.”
This study received support from various grants including those from the Judith and Stewart Colton Center for Autoimmunity at NYU Langone Health. Additionally, related patents have been filed by Dr. Wang and colleagues with plans for commercialization through Remunix Inc., a startup company formed by NYU Langone Health.
