Preclinical research led by Compugen's scientists together with Profs. Stephen Miller, Ph.D., and Joseph R. Podojil, Ph.D., both from the Department of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University2 , and published in an additional paper, demonstrates the potential of ILDR2-Fc fusion protein to address autoimmune and inflammatory conditions as well as the mechanism of action underlying this activity. The data show the potent and long-lasting immunomodulatory activity of ILDR2-Fc fusion protein in animal models of multiple sclerosis (R-EAE) and type 1 diabetes, and its ability to promote engraftment in an animal model of bone marrow transplantation. This work reveals the mechanism of action of ILDR2-Fc in ameliorating autoimmunity through regulation of immune homeostasis and re-establishment of immune tolerance to the disease-causing antigen, by the induction of regulatory T cells (Tregs).Prof. Miller commented, "Our findings point to a compelling mode of action for this Fc fusion protein in autoimmune diseases. In animals, this protein induced a long-term response following a short treatment duration through the promotion of regulatory T cells activating an immune tolerance induction mechanism. We also showed that this immune tolerance induction, addressing the autoimmune disease, is specific to the antigen driving the autoimmune disease and did not trigger a global non-specific inhibition of immune responses, thus potentially maintaining the immune response against infections and neo-malignancies."
- ILDR2 is a Novel B7-like Protein that Negatively Regulates T Cell Responses (Hecht et al, JI, in press)
- ILDR2-Fc is a Novel Regulator of Immune Homeostasis and Inducer of Antigen- Specific Immune Tolerance (Podojil et al, JI, in press)