Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 45, Issue 12, Pages 3302-3312Publisher
WILEY
DOI: 10.1002/eji.201545632
Keywords
alpha 4 beta 1-Integrin; CD8 T cell; Junctional adhesion molecule-B; Migration; Neuroinflammation
Categories
Funding
- international ARSEP grant
- Toulouse University Hospital
- French National Institute for Medical Research (INSERM)
- French National Research Agency [ANR-13-BSV3-0003-01]
- European Union, FP7-PEOPLE-2012-ITN NeuroKine
- Swiss National Science Foundation [149420]
- Swiss Multiple Sclerosis Society
- German Research Foundation
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Although CD8 T cells are key players in neuroinflammation, little is known about their trafficking cues into the central nervous system (CNS). We used a murine model of CNS autoimmunity to define the molecules involved in cytotoxic CD8 T-cell migration into the CNS. Using a panel of mAbs, we here show that the alpha 4 beta 1-integrin is essential for CD8 T-cell interaction with CNS endothelium. We also investigated which alpha 4 beta 1-integrin ligands expressed by endothelial cells are implicated. The blockade of VCAM-1 did not protect against autoimmune encephalomyelitis, and only partly decreased the CD8(+) T-cell infiltration into the CNS. In addition, inhibition of junctional adhesion molecule-B expressed by CNS endothelial cells also decreases CD8 T-cell infiltration. CD8 T cells may use additional and possibly unidentified adhesion molecules to gain access to the CNS.
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