Page 137 - Veterinary Immunology, 10th Edition

blood vessels. Changes in vascular endothelial cells are triggered
VetBooks.ir to a halt, integrins bind them firmly to vascular endothelial cells and
by tissue damage and microbial invasion. Selectins on endothelial
cells tether neutrophils and stimulate them to roll. When they come

signal the neutrophils to emigrate into tissues by passing through
the blood vessel walls.

Changes in Neutrophils

As neutrophils roll along the endothelial surface, a second set of
changes occurs. Platelet activating factor, chemokines, and
leukotrienes from the endothelial cells trigger the rolling
neutrophils to express the adhesive protein, leukocyte function–

associated antigen-1 (LFA-1). LFA-1 is an integrin that binds to an
intercellular adhesion molecule-1 (ICAM-1 or CD54) on endothelial
cells (Fig. 5.7). Their strong binding brings neutrophils to a
complete stop and attaches them firmly to the vessel wall, despite

the shearing force of the blood flow. After several hours,
endothelial cells activated by cytokines such as tumor necrosis
factor-α (TNF-α) express the strongly adhesive E-selectin (CD62E).
IL-1 and IL-23 also induce endothelial cells to produce chemokines

that attract still more neutrophils.

FIG. 5.7 A simplified view of the proteins and their ligands
engaged in neutrophil-vascular endothelial cell binding. Selectins
are carbohydrate-binding proteins that bind other glycoproteins.
This selectin-mediated binding is weak and temporary.
Subsequently, integrins on leukocytes, especially LFA-1, bind
strongly to their ligand ICAM-1 on vascular endothelial cells.
Elastase secreted by endothelial cells removes leukosialin, thus
permitting the neutrophil to bind strongly to the endothelial cell.

Integrins

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