About

Zsuzsanna Fabry is a Professor and Vice Chair of Research in the Department of Pathology and Laboratory Medicine at the University of Wisconsin School of Medicine and Public Health. Her research interests include immunopathology, neuroimmunology, and multiple sclerosis. She is involved in exploring the immune cells in the central nervous system and their pharmacological manipulation, contributing to understanding the roles of immune cells in tissue injury and repair in neurological conditions. Her work has been published in various scientific journals, highlighting her focus on the immune environment of the central nervous system and its implications for disease and therapy.

Research topics

• Biology
• Neuroscience
• Immunology
• Medicine
• Pathology
• Internal medicine
• Cell biology
• Computational biology
• Chemistry
• Anatomy

Selected publications

• VEGFR Blockade Reduces Mycobacterium tuberculosis-Induced Lung Pathology in Immunocompromised Mice

  Cells · 2026-03-24

  articleOpen access

  (Mtb) remains a significant public health threat, responsible for 1.6 million deaths in 2021. The development of new treatments is particularly urgent for immunocompromised individuals, including those with Mtb/HIV coinfection, who experience severe disease outcomes. Previous studies demonstrated that blockade of VEGFR1, a receptor expressed on monocytes that mediates their recruitment to infection sites, limits Mtb-induced pathology in immunocompetent mice of both Mtb-resistant (C57BL/6J) and Mtb-susceptible (B6.C3H-sst1) strains. The present study extends these findings by evaluating the VEGFR1/2 blockade strategy in immunocompromised hosts. Treatment with the VEGFR1/2 blocker SU5416 (semaxanib) reduced monocyte infiltration into the lungs of Mtb-infected immunocompromised RAG1KO mice without affecting bacterial protection. Reduced monocyte recruitment improved lung pathology. VEGFR1/2 blockade also decreased the number of NK cells in the lungs of RAG1KO mice. Notably, an elevated ratio and increased absolute number of neutrophil granulocytes were observed in the Mtb-infected lungs of both immunocompetent and immunocompromised mice following SU5416 administration. However, this increase in neutrophils did not exacerbate lung pathology, as most recruited granulocytes remained within the lung vasculature. The beneficial effect of VEGFR1/2 blockade in RAG1KO animals suggests that further investigation of VEGFR blockers, such as SU5416, as adjunctive therapy to anti-tuberculosis drug regimens for immunocompromised populations with tuberculosis is warranted.

  PublisherDOI

• Structural and Immunological Alterations at the Human Cribriform Plate in <i>Streptococcus pyogenes</i> Meningitis: A Case Study

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-30

  articleSenior author

  Abstract Streptococcus pyogenes or group A Streptococcus (GAS) meningitis is a rare but deadly infection with a high mortality. Its mechanisms of invasion are unknown, but it has been proposed to enter either through the cribriform plate olfactory nerve bundles or the blood brain barrier. Knowledge of how GAS impacts the cribriform plate olfactory nerves can help us better understand GAS pathogenesis and invasion, as well as how it impacts the olfactory nerve bundles. Here we present the case of a 39-year-old otherwise healthy man who presented to the local emergency department with altered mental status and expired the following day. Neuropathologic examination revealed bacterial leptomeningitis; blood and cerebrospinal fluid cultures both grew Streptococcus pyogenes . Examination of the cribriform plate was notable for perineural accumulation of GAS around certain olfactory nerve bundles. The accumulation around nerves seems to be random and not correlated to size. Nerves that are impacted by GAS as well as nerves that are not impacted display similar levels of gliosis markers GFAP and podoplanin. Neuropeptide Y, a neuropeptide that implicated in neuro-proliferation and hunger was found to colocalize with CD68 positive immune cells within the nasal epithelium, leading to speculations of its involvement in the inflammatory profile during this case of GAS meningitis. Cribriform plate skull channels had undergone width expansion within the patient, pointing towards local bone marrows involvement during infections. These findings are essential to better understanding the human cribriform plate’s role in CNS immune response and drainage.

  PublisherDOI

• Cribriform Plate Microenvironment Assembles a Suppressive Myeloid Network during EAE-induced Neuroinflammation

  eLife · 2026-02-25

  articleOpen accessSenior author

  During neuroinflammation, CD11c+CD11b+ myeloid cells accumulate at the cribriform plate, a key cerebrospinal fluid (CSF) and antigen outflow site in mice. At this site, podoplanin (PDPN)-expressing cells, including lymphatic vessels and meningeal layers, expand to create a distinct drainage microenvironment. In this study we sought to characterize myeloid cells which populate this region using a mouse model of neuroinflammation, experimental autoimmune encephalomyelitis (EAE). Utilizing a combination of immunohistochemistry, flow cytometry, and scRNAseq, we report that macrophages and dendritic cells (DCs) from this region display unique expressional signatures related to tolerance, cell death, and reduced inflammatory profile. Together this data supports that myeloid retention at the cribriform plate and olfactory bulb meninges promotes a local immunosuppressive environment.

  PublisherDOI

• Cribriform Plate Microenvironment Assembles a Suppressive Myeloid Network during EAE-induced Neuroinflammation

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-08

  articleOpen accessSenior author

  During neuroinflammation, CD11c+CD11b+ myeloid cells accumulate at the cribriform plate, a key cerebrospinal fluid (CSF) and antigen outflow site in mice. At this site, podoplanin (PDPN)-expressing cells, including lymphatic vessels and meningeal layers, expand to create a distinct drainage microenvironment. In this study we sought to characterize myeloid cells which populate this region using a mouse model of neuroinflammation, experimental autoimmune encephalomyelitis (EAE). Utilizing a combination of immunohistochemistry, flow cytometry, and scRNAseq, we report that macrophages and dendritic cells (DCs) from this region display unique expressional signatures related to tolerance, cell death, and reduced inflammatory profile. Together this data supports that myeloid retention at the cribriform plate and olfactory bulb meninges promotes a local immunosuppressive environment.

  PublisherDOI

• Author response: Cribriform Plate Microenvironment Assembles a Suppressive Myeloid Network during EAE-induced Neuroinflammation

  2026-02-25

  peer-reviewOpen accessSenior author
  PublisherDOI

• Cribriform Plate Microenvironment Assembles a Suppressive Myeloid Network during EAE-induced Neuroinflammation

  eLife · 2026-02-25

  articleOpen accessSenior author

  During neuroinflammation, CD11c+CD11b+ myeloid cells accumulate at the cribriform plate, a key cerebrospinal fluid (CSF) and antigen outflow site in mice. At this site, podoplanin (PDPN)-expressing cells, including lymphatic vessels and meningeal layers, expand to create a distinct drainage microenvironment. In this study we sought to characterize myeloid cells which populate this region using a mouse model of neuroinflammation, experimental autoimmune encephalomyelitis (EAE). Utilizing a combination of immunohistochemistry, flow cytometry, and scRNAseq, we report that macrophages and dendritic cells (DCs) from this region display unique expressional signatures related to tolerance, cell death, and reduced inflammatory profile. Together this data supports that myeloid retention at the cribriform plate and olfactory bulb meninges promotes a local immunosuppressive environment.

  PublisherDOI

• The role of neural progenitor cells in brain tuberculosis 4691

  The Journal of Immunology · 2025-11-01

  articleOpen access

  Abstract Description Tuberculosis (TB) of the central nervous system (CNS) is one of the rarest but highly destructive manifestations of Mycobacterium tuberculosis (Mtb) infection in humans. Only half of the patients survive and cognitive diseases are common. The existing knowledge about the infectious mechanisms and anti-mycobacterial immune responses in the brain is restricted by the lack of an optimal human CNS-TB model. In this research, we applied a new human in vitro model to investigate CNS-TB by infecting neural organoids and neural progenitor cells (NPC) with Mtb. Our research reveals that the phagocytic ability of NPCs towards Mtb offers a new perspective on CNS-TB studies. Internalized Mtb bacilli are found co-localized within late endosomal and phagolysosomal compartments, as well as in the cytoplasm of the NPCs. The Mtb infection induces NPC death and disrupts proliferation, further substantiating the pathological consequences of CNS-TB. Additionally, prominent type-1 IFN responses were observed in Mtb-infected NPCs. The treatments with anti-IFN alpha neutralization antibodies could partially rescue the NPCs from Mtb-induced proliferation impairments and cell death. Ultimately our findings demonstrate that these neural organoids and NPC-based in vitro systems offer a new approach for understanding the pathogenesis of CNS-TB and the associated learning deficiencies. Organoid cultures may offer a new platform for evaluating anti-mycobacterial treatment strategies for human CNS-TB. Topic Categories Immune Mechanisms of Human Disease (HUM)

  PublisherOA PDFDOI

• Characterization of the cribriform plate lymphatics in CNS Mtb infection 4556

  The Journal of Immunology · 2025-11-01

  articleOpen access

  Abstract Description CNS TB represents a severe, often life-threatening manifestation of Mycobacterium tuberculosis (Mtb) infection, characterized by significant neurological complications and high mortality. Development of cerebral edema leads to negative outcomes in CNS TB. Lymphatic drainage is crucial to remove metabolic waste products, reduce cranial pressure and present antigens in CNS inflammation. We have previously shown that meningeal lymphatic vessels near the cribriform plate (CP) undergo lymphangiogenesis during EAE-induced neuroinflammation and interact with leukocytes, creating an immunoregulatory niche. Here we show after CNS Mtb infection DCs enter the brain through the choroid plexus, followed by the recruitment of T cells, leading to IFNγ-mediated responses. We found infected DCs interacting with lymphatic endothelial cells (LEC) at the CP, indicating this region is an important drainage route and a possible immune regulatory check point. We measured lymphangiogenesis at the CP one-week post infection, which was inhibited by VEGFR-3 blockade, which also led to reduced IFNγ production by Mtb-specific CD4 T cells in the CNS. Using scRNAseq, we identified and compared LEC populations from Mtb-infected and sham-treated animals, which will lead to further understanding of the infection-mediated changes and immune regulatory functions of this lymphatic niche. Funding Sources Supported by NIH NS123449 to M.S., NIH NS126595 and NS108497 to Z.F. Topic Categories Neuroimmunology (NEUR)

  PublisherOA PDFDOI

• The cribriform plate: A dynamic central nervous system–immune hub

  The Journal of Experimental Medicine · 2025-11-27

  articleSenior author

  Olfactory nerve bundles exit the brain through the cribriform plate (CP) with a rich perineural microenvironment (cpPME). This microenvironment facilitates interactions between cerebrospinal fluid, blood vessels, bone marrow, and lymphatic vessels. The immune niche of the cpPME changes in response to inflammation caused by stroke, autoimmunity, infection, and Alzheimer's disease. Neuroinflammation at the CP results in dysfunction of olfaction that might have diagnostic value in neurological disorders. Additionally, the proximity of the CP to the nasal mucosa allows targeted therapeutic interventions. A thorough understanding of the cpPME is essential for designing innovative diagnostics and treatments for neuroinflammatory diseases.

  PublisherDOI

• Perineural immune environment of olfactory nerves is reshaped by neuroinflammatory drainage and connects to ethmoid bone marrow

  Science Advances · 2025-06-25 · 11 citations

  articleOpen accessSenior authorCorresponding

  Cerebrospinal fluid (CSF) contains inflammatory cues that enable peripheral immune surveillance of the central nervous system (CNS). While some cranial nerves allow for CSF efflux, the immune environment around CSF-interfacing cranial nerves during neuroinflammation is still poorly understood. Using a mouse model of multiple sclerosis [experimental autoimmune encephalomyelitis (EAE)] and CNS Mycobacterium tuberculosis infection (CNS-Mtb), we examined immune responses around olfactory nerve bundles near the cribriform plate, a key CSF efflux route. During neuroinflammation, we found increased perineural immune cells that had access to intracranial injected beads, dye, and bacteria. Additionally, we identified osseous channels connecting the environment surrounding olfactory nerves to bone marrow in the cribriform plate (cpBM). Notably, the cpBM undergoes myelopoiesis during EAE, has access to components of intracranial drainage, and is vulnerable to Mtb bacteria invasion during CNS-Mtb infection. Our findings improve the understanding of how the environments of CSF-interfacing cranial nerves and bone marrow are altered within the skull during neuroinflammatory disease.

  PublisherDOI

Recent grants

• CNS Tuberculosis

  NIH · $1.7M · 2012–2018

• NIH Grant R01NS037570

  NIH · $3.1M · 2014

• The role of T cells in ischemic brain damage

  NIH · $329k · 2017–2018

• NIH Grant R56NS037570

  NIH · $367k · 2009

• Role of T cells in ischemic brain damage

  NIH · $1.3M · 2018–2023

Frequent coauthors

• Mátyás Sándor

  Semmelweis University

  91 shared

• Martin Hsu

  University of North Carolina at Chapel Hill

  25 shared

• Aditya Rayasam

  Medical College of Wisconsin

  24 shared

• Melinda Herbáth

  University of Wisconsin–Madison

  24 shared

• Collin Laaker

  University of Wisconsin–Madison

  22 shared

• Jeffrey Harding

  21 shared

• Michael N. Hart

  Queen's University Belfast

  19 shared

• Melissa G. Harris

  17 shared