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The VLA-4/VCAM-1 molecules participate in gamma delta cell interaction with endothelial cells.
|Title||The VLA-4/VCAM-1 molecules participate in gamma delta cell interaction with endothelial cells.|
|Publication Type||Journal Article|
|Year of Publication||1992|
|Authors||Mohagheghpour N, Bermudez LE, Khajavi S, Rivas A|
|Date Published||1992 Aug|
|Keywords||Antigens, CD2, Antigens, Differentiation, T-Lymphocyte, Capillary Permeability, Cell Adhesion Molecules, Cell Communication, Cells, Cultured, Endothelium, Vascular, Humans, Lymphocyte Function-Associated Antigen-1, Receptors, Antigen, T-Cell, gamma-delta, Receptors, Immunologic, Receptors, Very Late Antigen, T-Lymphocytes, Vascular Cell Adhesion Molecule-1|
The accumulation of T lymphocytes at the site of chronic inflammation depends on a number of factors including adherence of T cells to vascular endothelial cells (EC) and endothelial permeability. We examined the effects of human gamma delta + T lymphocytes on the permeability of EC to macromolecules and characterized the cell surface molecules that are involved in these interactions. In this model, the flux of [125I]albumin was measured across the EC monolayer after a short-term culture with cloned gamma delta cells. Our results show that coculture of activated, but not resting, gamma delta cells with EC enhances endothelial permeability by a cytolytic process. Pretreating gamma delta cells with monoclonal antibodies directed at either LFA-1 or VLA-4 molecules or pretreating EC with monoclonal antibodies directed against either ICAM-1 or VCAM-1 molecules significantly inhibited gamma delta cell-mediated enhancement in endothelial permeability. This indicated that VLA-4/VCAM-1 and LFA-1/ICAM-1 adhesion pathways participate in gamma delta cell-EC interaction.
|Alternate Journal||Cell. Immunol.|