Commentary 10.1172/JCI95769

Astrocytes to the rescue! Glia limitans astrocytic endfeet control CNS inflammation

Francisco J. Quintana1,2

1Ann Romney Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA.

2The Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA.

Address correspondence to: Francisco J. Quintana, Ann Romney Center for Neurologic Diseases, Harvard Medical School, 60 Fenwood Road, Boston, Massachusetts 02115, USA. Phone: 617.525.5317; Email: fquintana@rics.bwh.harvard.edu.

Find articles by Quintana, F. in: JCI | PubMed | Google Scholar

First published July 24, 2017 - More info

Published in Volume 127, Issue 8 (August 1, 2017)
J Clin Invest. 2017;127(8):2897–2899. doi:10.1172/JCI95769.
Copyright © 2017, American Society for Clinical Investigation

First published July 24, 2017

See the related article at Astrocytic tight junctions control inflammatory CNS lesion pathogenesis.

The blood-brain barrier (BBB) and the glia limitans serve to prevent the migration of cells and other large molecules from the blood into the CNS. Neuroinflammatory diseases are characterized by disruption of the BBB and increased leukocyte infiltration into the CNS. In this issue of the JCI, Horng and colleagues demonstrate that astrocytes of the glia limitans induce tight junction formation in response to inflammatory cues, thereby tightening the border to limit the number of activated T cells infiltrating the CNS. Moreover, preventing the formation of this inducible barrier in mice increased disease severity in models of neuroinflammation. Together, the results of this study indicate that the inducible barrier of the glia limitans should be further explored as a therapeutic target.

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