Dr. Orly Avni joined Bar-Ilan University in 2012 from the Technion Institute of Technology. Prior to the Technion, she was a postdoctoral fellow at Harvard Medical School where she became an expert in the regulation of gene expression, especially in the immune system.
While the healthy function of the immune system is critical for combating infectious diseases, it is also essential for maintaining normal homeostasis of organs such as heart and brain. Dysregulation of gene expression in the immune system is associated with many diseases, such as autoimmune disorders, allergies, chronic inflammation, neurodegenerative disorders, heart failure, and cancer.
Today at the Bar-Ilan University Faculty of Medicine in the Galilee, Dr. Avni and her team are developing ways to scrutinize abnormalities in immune system regulation at the genomic and epigenetic levels and use this information to tailor precision therapies. Two of the more significant studies Dr. Avni and her team are focusing on are:
(i) The effects of social stress on the increased risk for autoimmune disorders;
(ii) Genetically inherited fatal cardiomyopathy, which is the result of a failure to tune cardiac response to common inflammatory stressors. Their research aims to develop new strategies for novel tailored-treatment modalities.
Annual Activity Report, March 2017 - The effects of social stress on immune regulation are imprinted on gut microbiota, and the implication of this for autoimmunity
Dys-biotic gut microbiota and psychological/social stress were both found to be associated with increased occurrence of autoimmune disorders, and we asked whether there might be a correlation. In a recent study, our results suggest that stress produces changes in growth and virulent-associated transcriptional patterns in selected stress-responsive indigenous bacterial communities. Certain white blood cells began to recognize indigenous bacteria as intruders transformed into more aggressive lymphocytes in order to attack them. This may jeopardize the normal tolerance to healthy tissue and increase the risk in individuals with a genetic predisposition to develop autoimmune disorders.