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Eur J Immunol. 2015 Dec;45(12):3302-12. doi: 10.1002/eji.201545632. Epub 2015 Oct 6.

Migration of encephalitogenic CD8 T cells into the central nervous system is dependent on the α4β1-integrin.

Author information

1
Department of Infectious and Tropical Diseases, Toulouse University Hospital, Toulouse, France.
2
INSERM U1043 - CNRS UMR 5282, Centre de Physiopathologie de Toulouse Purpan (CPTP), Toulouse, France.
3
Université Toulouse III, Toulouse, France.
4
Department of Clinical Neurosciences, Toulouse University Hospital, Toulouse, France.
5
Theodor Kocher Institute, University of Bern, Bern, Switzerland.

Abstract

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 α4β1-integrin is essential for CD8 T-cell interaction with CNS endothelium. We also investigated which α4β1-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.

KEYWORDS:

CD8 T cell; Junctional adhesion molecule-B; Migration; Neuroinflammation; α4β1-Integrin

PMID:
26358409
DOI:
10.1002/eji.201545632
[Indexed for MEDLINE]
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