BLTP3A (also known as UHRF1BP1) silenced CAR-T cells demonstrate elevated efficacy against High-grade serous carcinoma (HGSC)

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Impairing BLTP3A elevates T cells activity via enhanced recycling of TCR and CAR machinery through the endosomal system. 

Invention Summary:

Despite recent advances in cancer immunotherapy, objective responses remain rare. This is partly due to an incomplete understanding of the complex immunosuppressive mechanisms operating within the tumor microenvironment (TME).  

Rutgers researchers have discovered that an uncharacterized molecule expressed in T cells, BLTP3A suppresses protective T cell activities in the TME—and impairs the efficacy of TCR-T and CAR-T cellular Immunotherapeutics for cancer. The inventors use ablation or knockdown to downregulate BLTP3A expression, thereby enhancing T cell activity in cancer therapy. Unlike reprogramming metabolic strategies, impairing BLTP3A promotes enhanced avidity in targeting tumor antigens by promoting the retention of activating receptors on the T cell surface. 

Market Applications:

• Engineered tumor-antigen specific T cell in cancer treatment with enhanced function.  

• Improved effectiveness and fitness of T cell-based cellular therapeutics in cancer. 

Advantages:

• Ablation of BLTP3A in CD8 T cells delays tumor progression in an adoptive cell therapy model and may enhance responsiveness to anti-PD-1 checkpoint blockade, suggesting a promising therapeutic strategy. 

• Better survival outcomes in HGSC. 

Publications: •    Low-cost

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