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
PTC application pending
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