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Updated: Apr 18, 2026
Author Spotlight: Creating a Versatile Experimental Autoimmune Encephalomyelitis Model Relevant for Both Male and Female Mice
Published on: October 13, 2023
Dynamic changes in meningeal inflammation correspond to clinical exacerbations in a murine model of
Margaret E Walker-Caulfield1, Julianne K Hatfield1, Melissa A Brown1
1Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL, United States.
Abstract:
Inflammation in the meninges, tissues surrounding the brain and spinal cord that enclose the cerebrospinal fluid, closely parallels clinical exacerbations in relapsing-remitting experimental autoimmune encephalomyelitis (EAE). In preclinical disease, an influx of innate immune cells precedes loss of blood brain barrier (BBB) integrity and large-scale inflammation in the central nervous system (CNS). T cell infiltration into the meninges is observed in acute disease as well as during relapse, when neither BBB permeability nor significant increases in peripherally-derived immune cell numbers in the CNS are observed. These findings support the idea that the meninges are a gateway for immune cell access into the CNS, a finding that has important therapeutic implications.
Insights
Meningeal inflammation mirrors relapsing-remitting experimental autoimmune encephalomyelitis (EAE) exacerbations. The meninges act as a crucial gateway for immune cells entering the central nervous system (CNS), offering therapeutic insights.
Area of Science:
- Neuroimmunology
- Central Nervous System Inflammation
- Autoimmune Diseases
Background:
- Relapsing-remitting experimental autoimmune encephalomyelitis (EAE) is a model for multiple sclerosis.
- Meningeal inflammation correlates with disease activity in EAE.
- Immune cell infiltration into the central nervous system (CNS) is a hallmark of neuroinflammation.
Purpose of the Study:
- To investigate the role of meninges in immune cell trafficking into the CNS during EAE.
- To understand the sequence of events leading to CNS inflammation in EAE.
- To identify potential therapeutic targets for neuroinflammatory diseases.
Main Methods:
- Induction of EAE in a preclinical model.
- Monitoring of immune cell infiltration into the meninges and CNS.
- Assessment of blood-brain barrier (BBB) integrity.
- Analysis of T cell dynamics during different disease phases.
Main Results:
- Meningeal inflammation precedes BBB breakdown and CNS inflammation in preclinical EAE.
- T cell infiltration into the meninges occurs during acute EAE and relapse.
- Meningeal T cell infiltration is observed even without significant BBB permeability or increased CNS immune cells.
- The meninges serve as a critical site for immune cell entry into the CNS.
Conclusions:
- The meninges function as a key gateway for immune cell entry into the CNS.
- Targeting meningeal immune responses may offer a novel therapeutic strategy for CNS autoimmune diseases.
- Understanding meningeal immunity is crucial for developing treatments for neuroinflammatory conditions like EAE.
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