SUMMARY OF INVENTION
Interleukin-2 (IL-2) binds to the IL-2 receptor, and regulates gene expression mediated by the STAT5 family of transcription factors. This signaling pathway is crucial for the differentiation and maintenance of regulatory T (Treg) cells. For CD8+ T cells, IL-2 signals optimize both effector T (Teff) cell generation and differentiation into memory cells. Constitutively active STAT5 (STAT5-CA) relieves T-cell dependency on IL-2 signaling for their function.
MSK investigators have shown that expression of STAT5-CA in Treg cells augments Treg cell suppressor activity and significantly reduces organ-specific autoimmunity in mice. Based on these findings, expression of STAT5-CA in CD8+ Teff cells is expected to confer resistence to Treg cell-mediated suppression, and augment their anti-tumor activity.
These early-stage findings can inform the design of novel Treg cell-based therapies for a variety of autoimmune and inflammatory disorders and organ transplantation, and Teff cell-based therapies to treat cancer.
- Engineered Treg cells are novel cell therapies for autoimmune and inflammatory diseases
- Engineered Teff cells can improve the efficacy of existing T-cell based therapies, including CAR T-cells
- Exceptional scientific team with strong research background relating to regulatory T-cells
Based upon research to date, this novel technology offers broad potential for therapies relating to autoimmune disease and cancer
U.S. National application PCT/US2017/037794 published in October 2019; National applications also pending in Canada, Europe (published), Australia, China (published), Japan, and Hong Kong.
Chinen et al., An Essential Role for the IL-2 Receptor in Treg Cell Function. Nature Immunology, 2016 Nov; 17(11): 1322-1333, PMID: PMC5071159.
Alexander Rudensky, PhD, Chair, Immunology Program, Memorial Sloan Kettering; Director, Ludwig Center, MSK; Investigator, Howard Hughes Medical Institute