This research explores how elevated sialic acid levels impair T cell immunity in mitochondrial disease, proposing interventions to modulate sialic acid-Siglec interactions to improve antiviral responses. The study is at TRL 2, seeking to validate therapeutic potential in Ndufs4 KO mice.
This research targets the immune dysfunction observed in mitochondrial diseases, specifically focusing on elevated sialic acid levels that impair T cell antiviral immunity. By modulating the interactions between sialic acids and Siglecs, the study aims to enhance T cell function and improve recovery from viral infections. The findings could lead to novel therapeutic approaches for managing immune responses in mitochondrial disease patients.
The research is currently at TRL 2, focusing on exploring the fundamental interactions between sialic acids and Siglecs in T cell immunity. Future studies will validate therapeutic strategies in Ndufs4 KO mice to advance the project further.
The National Human Genome Research Institute is a U.S. federal biomedical research institute in Bethesda, Maryland, with a mission-driven, translational focus and a mix of intramural laboratories and collaborative programs. Corporate R&D teams engage through CRADAs and other NIH agreements, access shared core facilities and biorepositories, and collaborate on clinical studies at the NIH Clinical Center. The institute also stewards national data resources and advances standards that enable secure access, benchmarking, and validation. Research is backed by U.S. federal appropriations through NIH, with added support for collaborations via interagency and competitive mechanisms. Technology transfer uses NIH’s established IP, licensing, and CRADA pathways.