CD45 mAb Induces Cell Adhesion in Peripheral Blood Mononuclear Cells via Lymphocyte Function-Associated Antigen-1 (LFA-1) and Intercellular Cell Adhesion Molecule 1 (ICAM-1)

1993 ◽  
Vol 147 (1) ◽  
pp. 110-128 ◽  
Author(s):  
Hannes M. Lorenz ◽  
Thomas Harrer ◽  
Anand S. Lagoo ◽  
Andreas Baur ◽  
Gerhard Eger ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Peripheral Blood Mononuclear Cells ◽  
Cell Adhesion Molecule ◽  
Mononuclear Cells ◽  
Lymphocyte Function ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Cell Adhesion Molecule 1 ◽  
Intercellular Cell Adhesion Molecule

Adherence of adoptively transferred alloreactive Th1 cells in lung: partial dependence on LFA-1 and ICAM-1

2000 ◽  
Vol 279 (3) ◽  
pp. L583-L591 ◽  
Author(s):  
Anne E. Dixon ◽  
Janis B. Mandac ◽  
Paul J. Martin ◽  
Robert C. Hackman ◽  
David K. Madtes ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Lung Injury ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Th1 Cells ◽  
Lymphocyte Function ◽  
Vascular Cell Adhesion ◽  
Th1 Cell ◽  
Vascular Cell ◽  
Cell Adhesion Molecule 1

T helper type 1 (Th1) cells are important effectors in a number of immune-mediated lung diseases. We recently described a murine model of lung injury induced by adoptive transfer of cloned alloreactive Th1 cells. To investigate mechanisms that result in injury to the lung, we studied the in vivo distribution of 51Cr-labeled Th1 cells. One hour after intravenous administration, >85% of injected radioactivity was left in the lung, and at 24 h, 40% of radioactivity was left in the lung. Adherence of Th1 cells in the lung was significantly inhibited by neutralizing antibody to lymphocyte function-associated antigen-1. Th1 cell adherence also was decreased in lungs of mice deficient in intercellular adhesion molecule-1 (ICAM-1). Th1 cell transfer further induced expression of ICAM-1 and vascular cell adhesion molecule-1 in the lung. Vascular cell adhesion molecule-1-immunoreactive protein was markedly induced in lung endothelium by alloreactive Th1 cells. These findings indicate that Th1 cells localize in normal lung by a mechanism involving lymphocyte function-associated antigen-1 and ICAM-1. Alloreactive cells further induce endothelial adhesion molecules that may facilitate recruitment of inflammatory cells to the lung and amplify Th1 cell-induced lung injury.

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