Zsuzsanna Fabry

Credentials: PhD

Position title: Professor

Email: zfabry@wisc.edu

Phone: (608) 265-8716

Address:
6130 MSC
1300 University Ave
Madison, WI 53706

Lab
Fabry Lab

Focus Groups

Immunology/Immunopathology

Neuroscience/Neuropathology

Education

PhD, Immunology, Budapest, Hungary

Research Summary

Mechanisms of neuroinflammation in autoimmunity, infection or traumas of the Central Nervous System.

Research Detail

For the last several years, I have focused my research program on immune, traumatic and infectious diseases of the central nervous system (CNS) that are important for public health. Our goal is to improve strategies for treating CNS inflammation.

Multiple Sclerosis (MS) project: There are a number of important CNS human diseases of poorly understood autoimmune etiology which are characterized by the presence of inflammatory cell infiltrates in the CNS and immune-mediated disruption of CNS function. One example is Multiple Sclerosis (MS), which is a chronic inflammatory disease of the CNS. The pathogenesis of this disease is very difficult to understand. Our laboratory characterized several cellular and molecular factors that are involved in the regulation of dendritic cell and T-lymphocyte adhesion, migration and activation at the brain microvessel wall an in the CNS parenchyma. The goal of our studies is to understand the role of dendritic cells and T cells in CNS autoimmune inflammatory reactions and to design new treatment for CNS inflammatory diseases. Based on our in vitro studies, my team is participating in a National Multiple Sclerosis Society (NMSS) funded clinical trial to test novel therapies to treat humans with MS.

Central Nervous System Mycobacterium tuberculosis (Mtb) infection (CNSTB) project: One of the most dangerous infectious diseases of the CNS is caused by Mycobacterium tuberculosis (Mtb) (CNSTB). The World Health Organization (WHO) declared a tuberculosis (TB) global emergency and it is estimated that today 1/3 of the world population, or approximately 2 billion people, is infected with latent TB and CNSTB is on the rise. Despite its public health importance, current understanding about the pathogenesis of this disease is outdated and limited. The goal of our work is to study the pathogenesis of CNSTB. Our overall goals are to define the mechanisms of Mtb dissemination into the CNS and the nature of protective immunity in CNSTB. Our experiments will fill the gap in our knowledge regarding the pathogenesis of CNSTB and will lead to improved strategies for treating mycobacterial infections of the CNS.

CNS Stroke project: Stroke is one of the leading causes of death and disability worldwide. Clinical studies and preclinical experimental studies suggested the contribution of inflammation in acute and long-term neuronal tissue damage following ischemic stroke; however, the mechanisms and cells involved in stroke-induced neuroinflammation are not fully understood. We study the contribution of immune cells and mediators to stroke. Based on our preliminary data, we hypothesize that IL21 critically contributes to ischemic damage in the CNS. We aim to determine if IL-21 contributes to neuronal tissue injury in the post ischemic brain by activating specific immune cells, damaging the blood-brain barrier and inducing neuronal death.

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