Elsevier

Cellular Immunology

Volume 129, Issue 1, August 1990, Pages 125-137
Cellular Immunology

ICAM-1-dependent fibroblast-lymphocyte adhesion: Discordance between surface expression and function of ICAM-1

https://doi.org/10.1016/0008-8749(90)90192-TGet rights and content

Abstract

We have previously reported that stimulation of human fibroblasts (FB) with interferon-γ (IFN-γ) leads to their increased adhesiveness for resting peripheral blood T lymphocytes. With the use of blocking monoclonal antibodies, we determined that intercellular adhesion molecule-1 (ICAM-1) and its T cell ligand, lymphocyte function-associated antigen-1 (LFA-1) are the major, if not only ligands involved in this system. Using an ELISA, we have confirmed earlier reported observations that IFN-γ induces an increase of ICAM-1 expression on the surface of FB suggesting that this increase mediates lymphocyte adhesion. However, we show that treatment of FB with IL-1, while leading to comparable increases in ICAM-1 synthesis and expression, failed to induce increased adhesion. In contrast, treatment of fibroblasts with the phorbol ester, TPA, stimulated ICAM-1-dependent adhesion without an increase in ICAM-1 surface expression. This suggested that the detection of ICAM-1 by monoclonal antibody techniques may not always correlate with its functional capabilities. The contrasting effects of IFN-γ and IL-1 on ICAM-1-dependent FB adhesion suggest that qualitative as well as quantitative alterations of the ICAM-1 molecule may regulate ligand interaction.

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    Supported by a grant from the Medical Research Service of the Veterans Administration, Grants AR32343 and AR20621 from the USPHS, and a grant from the Connecticut Chapter of the Arthritis Foundation.

    1

    T.H.P. was supported by an NIH postdoctoral training grant (AR07475).

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