Immune cells begin to populate the central nervous system (CNS) already during embryonic development. The cells, termed microglia, become permanent residents of the tissue with a variety of functions such as clearance of pathogens and regulation of neuronal function. We address questions related to their unique differentiation process following entry into the CNS as well as their impact on chronic diseases of the brain such as epilepsy, multiple sclerosis and Alzheimerâ€™s disease.
Alzheimerâ€™s disease is characterized by enhanced degeneration processes of the aging brain, which lead to cognitive decline and dementia. Our goal is to reveal immune mechanisms contributing to AD pathogenesis and thereby to develop immune-based early biomarkers and therapeutic approaches.
Chronic stress may alter the homeostatic functioning of the immune system by altering cellular responses to glucocorticoids. Such imbalance of immune regulation may then exacerbate or predispose to chronic illnesses such as depression, autoimmunity and neurodegenerative diseases. Our studies address the regulatory role of glucocorticoids in leukocyte and endothelial subsets and how such regulation is impaired following chronic stress or chronic inflammation.
Although the etiology of autoimmune diseases is mostly unknown, it is becoming clear that a loss in immune regulation results in pathogenic stimulation of autoreactive lymphocytes which otherwise kept quiescent. Once such pathogenic stimulation of lymphocytes occurs, the cells can renew and continuously attack the body. Our research, in collaboration with Prof. Smadar Cohen, is aimed at generating transplantable lymphoid-like scaffolds which attenuate the function of pathogenic T cells and hence allow to preserve essential tissue functions.