scFv(TACSTD2)-CD28-CD3zeta CAR-T Lentivirus

The scFv(TACSTD2)-CD28-CD3zeta CAR-T Lentivirus is a high-titer, replication-incompetent viral vector designed for the genetic modification of T cells to target Tumor-Associated Calcium Signal Transducer 2 (TACSTD2), commonly known as TROP2. The vector carries a second-generation Chimeric Antigen Receptor (CAR) construct, which consists of an antigen-binding scFv derived from a TROP2-specific monoclonal antibody, a CD28 costimulatory domain, and a CD3-zeta signaling domain. TROP2 is a cell-surface glycoprotein overexpressed in various solid tumors, including breast, lung, and pancreatic cancers, while showing limited expression in normal tissues. By utilizing a lentiviral delivery system, the CAR gene is stably integrated into the host T cell genome, allowing for persistent receptor expression across cell generations. This architecture is specifically engineered to trigger robust T cell activation and expansion upon binding to the target antigen, bypassing the need for traditional MHC-restricted antigen presentation.

In practical research settings, this lentiviral product is essential for the production of TROP2-redirected CAR-T cells for preclinical validation and therapeutic development. It is primarily used to evaluate the cytotoxic potential of engineered T cells against TROP2-positive tumor cell lines through in vitro assays measuring cell lysis and inflammatory cytokine release, such as IFN-gamma and IL-2. Beyond cell-based assays, the virus enables the creation of CAR-T cells for in vivo studies using patient-derived or cell-line-derived xenograft models to assess tumor infiltration, persistence, and overall anti-tumor efficacy. Additionally, this tool is valuable for investigating the influence of the CD28 costimulatory domain on T cell metabolism and memory formation. Researchers also utilize this system to explore synergistic effects when combining CAR-T cells with checkpoint inhibitors or other pharmacological agents to overcome the immunosuppressive challenges of the tumor microenvironment.