As with other types of leukocytes, mechanisms that function to enable
the recruitment of eosinophils into specific sites of immune reactions
involve a complex and cumulative interplay of many molecules and path
ways. No single chemoattractant is specific for eosinophils, but rathe
r various chemoattractants active on eosinophils can also elicit migra
tion of other specific cell types. Humoral mediators causing eosinophi
l migration include C5a and platelet-activating factor, whereas cytoki
nes active as eosinophil chemoattractants include interleukin (IL)-2,
IL-3, IL-5, granulocyte/macrophage colony-stimulating factor, lymphocy
te chemoattractant factor, and RANTES. Eosinophils utilize several pat
hways to adhere to vascular endothelial cells, including binding to in
tercellular adhesion molecule-1, E-selectin, and vascular cell adhesio
n molecule-1 (VCAM-1). The lack of binding of neutrophils to VCAM-1 an
d the enhanced expression of VCAM-1 elicited by IL-4 contribute to pre
ferential eosinophil accumulation. Eosinophil recruitment is dependent
not only on ligands expressed on eosinophils and molecules inducible
on endothelial cells but also on processes active during transendothel
ial migration and extravascular migration in the extracellular spaces.