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Impaired transendothelial migration of B-CLL lymphocytes: a defect linked to low L-selectin expression
1Sydney University, Department of Medicine, Nepean Hospital, Penrith, NSW 2750, Australia.
The emigration of lymphocytes from blood into lymph nodes is regulated by the expression of the adhesion molecule, L-selectin on the lymphocyte surface which arrests the rolling of the cell on the vessel wall and allows firmer adhesive interactions to develop. The expression of L-selectin on B-CLL lymphocytes is less than half that on normal lymphocytes and this difference correlates with an impaired capacity of B-CLL lymphocytes to migrate beneath a monolayer of human umbilical vein endothelial cells. Both the B-cell and T-cell lymphocytes from normal subjects and B-CLL patients show down-regulation of L-selectin and CD23 after transendothelial migration. The reduced expression of L-selectin on B-CLL lymphocytes leads to a relative "trapping" of these cells in the vascular space and is one factor contributing to the elevation of peripheral lymphocyte count.
The emigration of lymphocytes from blood into lymph nodes is regulated by the expression of the adhesion molecule, L-selectin on the lymphocyte surface which arrests the rolling of the cell on the vessel wall and allows firmer adhesive interactions to develop. The expression of L-selectin on B-CLL lymphocytes is less than half that on normal lymphocytes and this difference correlates with an impaired capacity of B-CLL lymphocytes to migrate beneath a monolayer of human umbilical vein endothelial cells. Both the B-cell and T-cell lymphocytes from normal subjects and B-CLL patients show down-regulation of L-selectin and CD23 after transendothelial migration. The reduced expression of L-selectin on B-CLL lymphocytes leads to a relative "trapping" of these cells in the vascular space and is one factor contributing to the elevation of peripheral lymphocyte count.

