Cooperative interactions of LFA-1 and Mac-1 with intercellular adhesion molecule-1 in facilitating adherence and transendothelial migration of human neutrophils in vitro. (original) (raw)
Research Article Free access | 10.1172/JCI114111
Speros P. Martel Laboratory of Leukocyte Biology, Baylor College of Medicine, Houston, Texas 77054.
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Speros P. Martel Laboratory of Leukocyte Biology, Baylor College of Medicine, Houston, Texas 77054.
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Speros P. Martel Laboratory of Leukocyte Biology, Baylor College of Medicine, Houston, Texas 77054.
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Speros P. Martel Laboratory of Leukocyte Biology, Baylor College of Medicine, Houston, Texas 77054.
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Speros P. Martel Laboratory of Leukocyte Biology, Baylor College of Medicine, Houston, Texas 77054.
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Published June 1, 1989 -More info
Published June 1, 1989 -Version history
The adherence of human neutrophils to human umbilical vein endothelial cells (HUVEC) is partially dependent on the CD11/CD18 family of glycoproteins on the neutrophil and ICAM-1 on the HUVEC. The CD18 heterodimer involved in this adherence was evaluated in vitro using subunit-specific monoclonal antibodies (MAbs). The adherence of unstimulated neutrophils to IL-1-stimulated HUVEC was significantly inhibited by anti-CD11a but not CD11b MAbs, while the adherence of fMLP-stimulated neutrophils was significantly inhibited by both anti-CD11a and -CD11b. Anti-CD11a, but not anti-CD11b MAbs, reduced the adherence of unstimulated neutrophils on purified ICAM-1 to the same low level untreated neutrophils exhibited on a control protein, glycophorin. Stimulation with fMLP significantly increased neutrophil attachment to purified ICAM-1, but not to the control protein. Anti-CD11b MAbs reduced this chemotactically augmented adherence to that of unstimulated neutrophils, and in combination with anti-CD11a MAbs reduced adherence to that on the control protein. The results in this report indicate that unstimulated neutrophils exhibit LFA-1-dependent attachment to ICAM-1, and chemotactic stimulation enhances the attachment of human neutrophils to ICAM-1 by a Mac-1-dependent process.
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