Eur J Immunol 2002 Dec;32(12):3598-606
Laschinger M, Vajkoczy E.
Max-Planck-Institute for Physiological and Clinical Research, Bad Nauheim,
Germany.
LFA-1 on the surface of encephalitogenic T cells has been suggested to be involved in the pathogenesis of experimental autoimmune encephalomyelitis.
By applying a novel technique of intravital fluorescence microscopy that enables us to visualize the interaction of circulating encephalitogenic T lymphoblasts within the healthy spinal cord white matter microvasculature in vivo, we investigated the possible involvement of LFA-1 on circulating encephalitogenic T cells in their multi-step interaction with the blood-brain barrier endothelium in vivo.
LFA-1 was found to mediate neither the G-protein-independent capture nor the G-protein-dependent initial adhesion strengthening of encephalitogenic T cell blasts within spinal cord microvessels.
In contrast, blocking of LFA-1 on encephalitogenic T lymphoblasts resulted in a significantly reduced number of T cells firmly adhering within spinal cord microvessels 2 h after injection and in a significantly reduced number of T cells subsequently migrating across the vascular wall into the spinal cord parenchyme.
Our study provides the first direct evidence that encephalitogenic T cells use LFA-1 for transendothelial migration but not for capture and initial adhesion in spinal cord microvessels in vivo.