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Monocyte Adhesion to Xenogeneic Endothelium during Laminar Flow Is Dependent on -Gal-Mediated Monocyte Activation¹

Mark D. Peterson^*,, Rongyu Jin, Sharon Hyduk, Pascal Duchesneau, Myron I. Cybulsky and Thomas K. Waddell^2,,

^* Division of Cardiac Surgery, Department of Surgery, Department of Laboratory Medicine and Pathobiology, Division of Thoracic Surgery, Toronto General Hospital Research Institute, University Health Network, University of Toronto, Toronto, Ontario, Canada

Monocytes are the predominant inflammatory cell recruited to xenografts and participate in delayed xenograft rejection. In contrast to allogeneic leukocytes that require up-regulation of endothelial adhesion molecules to adhere and emigrate into effector tissues, we demonstrate that human monocytes adhere rapidly to unstimulated xenogeneic endothelial cells. The major xenoantigen galactose(1,3)galactose(1,4)GlcNAc-R (-gal) is abundantly expressed on xenogeneic endothelium. We have identified a putative receptor for -gal on human monocytes that is a member of the C-type family of lectin receptors. Monocyte arrest under physiological flow conditions is regulated by -gal, because cleavage or blockade results in a dramatic reduction in monocyte adhesion. Recruitment of human monocytes to unactivated xenogeneic endothelial cells requires both ₄ and ₂ integrins on the monocyte; binding of -gal to monocytes results in rapid activation of ₂, but not ₄, integrins. Thus, activation of monocyte ₂ integrins by -gal expressed on xenogeneic endothelium provides a mechanism that may explain the dramatic accumulation of monocytes in vivo.

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The JI 2005 174: 7477-7478. [Full Text]  

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