With LRI funding, Dr. Kotzin and his colleague Stephen J. Rozzo, PhD, successfully developed genetically altered mouse models to study the role of Type I interferon in the cause and development of lupus.
Using sophisticated mouse-breeding experiments, Dr. Rozzo showed that one of the genes on chromosome number one—Interferon Inducible 202 (Ifi202)—may regulate the intensity of organisms' immune responses. The interferons are chemicals that immune cells produce to communicate with each other.
They zeroed in on a gene that appears to play a significant role in lupus. By testing whether this is the case and characterizing the mechanism by which this gene contributes to autoimmune disease, their research has defined, with unprecedented precision, potentially important targets for treating the disease.
New studies will determine whether genetic deficiency or suppression of interferon action prevents disease expression.