Neuroinflammation-induced lymphangiogenesis near the cribriform plate contributes to drainage of CNS-derived antigens and immune cells

Martin Hsu, Aditya Rayasam, Julie A. Kijak, Yun Hwa Choi, Jeffrey S. Harding, Sarah A. Marcus, William J. Karpus, Matyas Sandor and Zsuzsanna Fabry ()
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Martin Hsu: University of Wisconsin-Madison
Aditya Rayasam: University of Wisconsin-Madison
Julie A. Kijak: University of Wisconsin-Madison
Yun Hwa Choi: University of Wisconsin-Madison
Jeffrey S. Harding: Mount Sinai Hospital
Sarah A. Marcus: University of Wisconsin-Madison
William J. Karpus: University of Wisconsin-Madison
Matyas Sandor: University of Wisconsin-Madison
Zsuzsanna Fabry: University of Wisconsin-Madison

Nature Communications, 2019, vol. 10, issue 1, 1-14

Abstract: Abstract There are no conventional lymphatic vessels within the CNS parenchyma, although it has been hypothesized that lymphatics near the cribriform plate or dura maintain fluid homeostasis and immune surveillance during steady-state conditions. However, the role of these lymphatic vessels during neuroinflammation is not well understood. We report that lymphatic vessels near the cribriform plate undergo lymphangiogenesis in a VEGFC – VEGFR3 dependent manner during experimental autoimmune encephalomyelitis (EAE) and drain both CSF and cells that were once in the CNS parenchyma. Lymphangiogenesis also contributes to the drainage of CNS derived antigens that leads to antigen specific T cell proliferation in the draining lymph nodes during EAE. In contrast, meningeal lymphatics do not undergo lymphangiogenesis during EAE, suggesting heterogeneity in CNS lymphatics. We conclude that increased lymphangiogenesis near the cribriform plate can contribute to the management of neuroinflammation-induced fluid accumulation and immune surveillance.

Date: 2019
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DOI: 10.1038/s41467-018-08163-0

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