About

Matyas Sandor is a Professor in the Department of Pathology and Laboratory Medicine at the University of Wisconsin School of Medicine and Public Health. His research focuses on immune responses to infectious diseases, particularly the role of T cells in granulomatous immune responses induced by infectious agents such as Schistosoma mansoni, Leishmania donovani, and Mycobacterium bovis. He studies how granulomas, which are localized inflammatory reactions containing both T cells and infectious agents, protect the host against infection but can also contribute to diseases like sarcoidosis and Crohn's disease. His work involves examining how T cells fight chronic infections using T cells from TCR transgenic mice and infectious agents transfected with specific antigens, as well as investigating how different T cell populations work together. Additionally, he explores how antibodies and effector pathways mediated by complement and Fc receptors interfere with T cell responses, with the aim of contributing to the development of better vaccines and treatments for granulomatous diseases.

Research topics

• Neuroscience
• Computational biology
• Biology

Selected publications

• Modeling infectious diseases of the central nervous system with human brain organoids

  Translational research · 2022 · 8 citations

  Senior authorCorresponding
  • Neuroscience
  • Biology
  • Computational biology
  PublisherOA PDFDOI

• Neuroinflammation creates an immune regulatory niche at the meningeal lymphatic vasculature near the cribriform plate

  Nature Immunology · 2022 · 74 citations

  • Biology
  • Cell biology
  • Pathology
  PublisherOA PDFDOI

• CXCL13 expressed on inflamed cerebral blood vessels recruit IL-21 producing TFH cells to damage neurons following stroke

  Journal of Neuroinflammation · 2022 · 35 citations

  • Neuroscience
  • Medicine
  • Immunology

  BACKGROUND: Ischemic stroke is a leading cause of mortality worldwide, largely due to the inflammatory response to brain ischemia during post-stroke reperfusion. Despite ongoing intensive research, there have not been any clinically approved drugs targeting the inflammatory component to stroke. Preclinical studies have identified T cells as pro-inflammatory mediators of ischemic brain damage, yet mechanisms that regulate the infiltration and phenotype of these cells are lacking. Further understanding of how T cells migrate to the ischemic brain and facilitate neuronal death during brain ischemia can reveal novel targets for post-stroke intervention. METHODS: To identify the population of T cells that produce IL-21 and contribute to stroke, we performed transient middle cerebral artery occlusion (tMCAO) in mice and performed flow cytometry on brain tissue. We also utilized immunohistochemistry in both mouse and human brain sections to identify cell types and inflammatory mediators related to stroke-induced IL-21 signaling. To mechanistically demonstrate our findings, we employed pharmacological inhibitor anti-CXCL13 and performed histological analyses to evaluate its effects on brain infarct damage. Finally, to evaluate cellular mechanisms of stroke, we exposed mouse primary neurons to oxygen glucose deprivation (OGD) conditions with or without IL-21 and measured cell viability, caspase activity and JAK/STAT signaling. RESULTS: cells in the ischemic brain. We also illustrate that neurons express IL-21R in the peri-infarct regions of both mice and human stroke tissue in vivo. Lastly, we found that IL-21 acts on mouse primary ischemic neurons to activate the JAK/STAT pathway and induce caspase 3/7-mediated apoptosis in vitro. CONCLUSION: These findings identify a novel mechanism for how pro-inflammatory T cells are recruited to the ischemic brain to propagate stroke damage and provide a potential new therapeutic target for stroke.

  PublisherOA PDFDOI

• Molecular Mechanisms of Neuroimmune Crosstalk in the Pathogenesis of Stroke

  International Journal of Molecular Sciences · 2021 · 61 citations

  • Neuroscience
  • Immunology
  • Medicine

  Stroke disrupts the homeostatic balance within the brain and is associated with a significant accumulation of necrotic cellular debris, fluid, and peripheral immune cells in the central nervous system (CNS). Additionally, cells, antigens, and other factors exit the brain into the periphery via damaged blood-brain barrier cells, glymphatic transport mechanisms, and lymphatic vessels, which dramatically influence the systemic immune response and lead to complex neuroimmune communication. As a result, the immunological response after stroke is a highly dynamic event that involves communication between multiple organ systems and cell types, with significant consequences on not only the initial stroke tissue injury but long-term recovery in the CNS. In this review, we discuss the complex immunological and physiological interactions that occur after stroke with a focus on how the peripheral immune system and CNS communicate to regulate post-stroke brain homeostasis. First, we discuss the post-stroke immune cascade across different contexts as well as homeostatic regulation within the brain. Then, we focus on the lymphatic vessels surrounding the brain and their ability to coordinate both immune response and fluid homeostasis within the brain after stroke. Finally, we discuss how therapeutic manipulation of peripheral systems may provide new mechanisms to treat stroke injury.

  DOI

• CNS lymphangiogenesis regulates fluid homeostasis and immunity during neuroinflammation

  The Journal of Immunology · 2020

  • Pathology
  • Anatomy
  • Medicine

  Abstract Recent reports have described meningeal lymphatic vessels residing in the dural layer surrounding the dorsal and basal regions of the brain as well as near the cribriform plate. While all three regions are able to uptake CSF macromolecules, it is unknown how cells and fluid from the CSF-filled subarachnoid space gain access through the blood-CSF arachnoid barrier and into dural lymphatics. In this study, we expand on our previous findings demonstrating the capability of neuroinflammation-induced cribriform plate lymphangiogenic vessels in draining CSF and leukocytes. These lymphatics reside in an optimal location for CSF drainage due to gaps in the arachnoid epithelial layer separating the dura from the subarachnoid space and correlate with increased CSF accumulation near the cribriform plate during neuroinflammation. This is in contrast to other lymphatics residing in the dural layer dorsal and basal to the brain, which are separated from CSF by a complete and uninterrupted arachnoid layer. Additionally, we show lymphangiogenic cribriform plate lymphatic vessels dynamically up-regulate proteins to increase dendritic cell binding and T-cell tolerance during autoimmunity. These data identify cribriform plate lymphatic vessels as dynamic structures that are able to undergo lymphangiogenesis to facilitate fluid drainage and regulate adaptive immunity during neuroinflammation.

  PublisherDOI

Frequent coauthors

• Diane Sewell

  University of Wisconsin–Madison

  2 shared

• Karin R. Swartz

  Medical College of Wisconsin

  2 shared

• Zsuzsanna Fábry

  University of Wisconsin–Madison

  2 shared

• Qing Zhu

  Sichuan University

  1 shared

• Collin Laaker

  University of Wisconsin–Madison

  1 shared

• Eva G. Rakasz

  University of Wisconsin–Madison

  1 shared

• Thanthrige Thiunuwan Priyathilaka

  University of Wisconsin–Madison

  1 shared

• Melinda Herbath

  University of Wisconsin–Madison

  1 shared

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