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Departments of Pediatrics, Microbiology-Immunology, and Pathology, Dalhousie University, Halifax, Nova Scotia, Canada
T lymphocyte infiltration into inflamed tissues is thought to
involve lymphocyte rolling on vascular endothelial cells. Because both
selectin and 
4 integrin adhesion molecules can mediate
leukocyte rolling, the contribution of these receptors to lymphocyte
migration to inflammation was examined. The recruitment of
111In-labeled spleen T cells to intradermal sites injected
with IFN-
, TNF-, LPS, poly inosine-cytosine, and Con A was
measured in the rat, and the effect of blocking mAbs to E-selectin,
P-selectin, very late activation Ag-4 (VLA-4), and LFA-1 was determined
on this T cell migration in vivo. Anti-E-selectin and
anti-P-selectin mAbs each inhibited 10–40 and 20–48%,
respectively, of the T lymphocyte migration to the inflammatory sites,
depending on the stimulus. Blocking VLA-4 inhibited 50% of the
migration to all of the lesions except Con A. Treatment with both
anti-VLA-4 and anti-E-selectin mAbs inhibited up to 85% of the
lymphocyte accumulation, while P-selectin and VLA-4 blockade in
combination was not more effective than VLA-4 blockade alone in
TNF-, IFN-, LPS, and poly inosine-cytosine lesions. Inhibiting
E-selectin, P-selectin, and VLA-4 together nearly abolished lymphocyte
migration to all inflammatory sites. Anti-LFA-1 mAb strongly inhibited
lymphocyte accumulation by itself, and this inhibition was not
significantly further reduced by E- or P-selectin blockade. Thus, T
cell migration to dermal inflammation is dependent on E-selectin,
P-selectin, and VLA-4, likely because these three receptors are
required for rolling of memory T lymphocytes, but VLA-4 and E-selectin
are especially important for lymphocyte infiltration in these
tissues.
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