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PS binding molecules could restore inactive or memory T cell functions.
Invention Summary:
Phosphatidylserine (PS) exposure on the cell surface is often a signal for phagocytosis and can lead to an immunosuppressive effect. Therefore, its inhibition by PS-binding biomolecules can promote a more immuno-responsive microenvironment. However, there is no prior evidence showing that PS-binding molecules are capable of restoring the effector function of antigen non-responsive or exhausted memory T cells.
Rutgers researchers discovered that PS-binding molecules could increase the number of antigen responsive functional T cells by downregulating several checkpoints on their surface. This provides a means to enhance the diagnostic sensitivity of latent TB assays and has potential immunotherapeutic implications in individuals with compromised T cell immunity. Additionally, this innovation suggests the possible use of PS binding molecule as an adjuvant with vaccine antigens to induce long-lasting immunity
Market Applications:
- Improve the sensitivity of available TB test
- Increased number of antigen or neoantigen activated T cells for therapeutic use in different diseases, such as viral infections and cancer.
Advantages:
- Improve sensitivity to detect latent and extrapulmonary TB infection.
- Target activation of antigen specific T cells.
Intellectual Property & Development Status: Provisional application filed. Patent pending. Available for licensing and/or research collaboration. For any business development and other collaborative partnerships, contact: marketingbd@research.rutgers.edu
