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Migration of encephalitogenic CD8 T cells into the central nervous system is dependent on the ?4?1-integrin.


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 ?4?1-integrin is essential for CD8 T-cell interaction with CNS endothelium. We also investigated which ?4?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.

SUBMITTER: Martin-Blondel G 

PROVIDER: S-EPMC7163664 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature

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

Martin-Blondel Guillaume G   Pignolet Béatrice B   Tietz Silvia S   Yshii Lidia L   Gebauer Christina C   Perinat Therese T   Van Weddingen Isabelle I   Blatti Claudia C   Engelhardt Britta B   Liblau Roland R  

European journal of immunology 20151006 12


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  ...[more]

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