UMMS Affiliation

Department of Pathology

Publication Date


Document Type



Immune System Diseases | Immunopathology | Molecular and Cellular Neuroscience | Nervous System Diseases


Multiple Sclerosis (MS) is an inflammatory disease of the Central Nervous System (CNS) that causes the demyelination of nerve cells and destroys oligodendrocytes, neurons and axons. Historically, MS has been thought of as a T cell-mediated autoimmune disease of CNS white matter. However, recent studies have identified gray matter lesions in MS patients, suggesting that CNS antigens other than myelin proteins may be involved during the MS disease process. We have recently found that T cells targeting astrocyte-specific antigens can drive unique aspects of inflammatory CNS autoimmunity, including the targeting of gray matter and white matter of the brain and inducing heterogeneous clinical disease courses. In addition to being a target of T cells, astrocytes play a critical role in propagating the inflammatory response within the CNS induced NF-kappaB signaling. Here, we will discuss the pathophysiology of CNS inflammation mediated by T cell-glial cell interactions and its contributions to CNS autoimmunity.


T cell, astrocytes, autoimmunity, cerebellum, experimental autoimmune encephalomyelitis, glial fibrillary acidic protein, multiple sclerosis

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Copyright © 2015 Huseby, Kamimura, Arima, Parello, Sasaki and Murakami. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

DOI of Published Version



Front Cell Neurosci. 2015 Aug 5;9:295. doi: 10.3389/fncel.2015.00295. eCollection 2015. Link to article on publisher's site

Journal/Book/Conference Title

Frontiers in cellular neuroscience

Related Resources

Link to Article in PubMed

PubMed ID


Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.