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Blood, 15 June 2006, Vol. 107, No. 12, pp. 4721-4727.
Prepublished online as a Blood First Edition Paper on February 9, 2006; DOI 10.1182/blood-2005-11-4683.
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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
ICAM-2 mediates neutrophil transmigration in vivo: evidence for stimulus specificity and a role in PECAM-1–independent transmigration
Miao-Tzu Huang,
Karen Y. Larbi,
Christoph Scheiermann,
Abigail Woodfin,
Nicole Gerwin,
Dorian O. Haskard, and
Sussan Nourshargh
From the Cardiovascular Medicine Unit, National Heart & Lung Institute, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, United Kingdom; and DG Thrombotic/Degenerative Joint Diseases, Aventis Pharma Deutschland, Frankfurt am Main, Germany.
ICAM-2 has been implicated in leukocyte transmigration in vitro, but there is little in vivo evidence to support this. To address this, neutrophil migration was investigated in ICAM-2–deficient mice (KO) and in wild-type (WT) mice treated with an anti–ICAM-2 blocking monoclonal antibody (mAb) (3C4). In a peritonitis model, IL-1 –induced accumulation of neutrophils was significantly reduced in mice treated with 3C4 (51% inhibition) and in KO mice (41% inhibition). In contrast, TNF- – or thioglycolate-induced responses were not suppressed in KO mice. Analysis of IL-1–induced leukocyte responses in cremasteric venules of KO animals by intravital microscopy indicated a defect in transmigration (44% inhibition) but not rolling or adhesion. As found before, TNF-–induced leukocyte transmigration was unaltered in the KO mice. WT mice treated with the anti–ICAM-2 mAb also exhibited a selective reduction in leukocyte transmigration in response to IL-1 while an anti–ICAM-1 mAb inhibited both leukocyte adhesion and transmigration. Interestingly, mAb 3C4 significantly suppressed IL-1–induced neutrophil transmigration in PE-CAM-1 KO animals in the peritonitis model but not in the cremaster muscle. The findings provide direct evidence for the involvement of ICAM-2 in neutrophil transmigration in vivo, though this role appears to be stimulus specific. Furthermore, ICAM-2 appears capable of mediating PECAM-1–independent leukocyte transmigration.
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