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Interleukin-4 induces homotypic aggregation of human mast cells by
promoting LFA-1/ICAM-1 adhesion molecules
H Toru, T Kinashi, C Ra, S Nonoyama, J Yata and T Nakahata
Department of Pediatrics, School of Medicine, Tokyo Medical and Dental
University, Bunkyo-ku, Japan.
We report here that interleukin-4 (IL-4) induces homotypic aggregation of
cultured human mast cells, grown from cord blood mononuclear cells in the
presence of stem cell factor and IL-6. This aggregation was specifically
induced by IL-4, because other cytokines including IL- 1alpha, IL-1beta,
IL-2, IL-3, IL-5, IL-9, IL-10, interferon-gamma, IL- 12,
granulocyte-macrophage colony-stimulating factor, NGF-beta, and tumor
necrosis factor-alpha failed to show such effect. Flow cytometric analysis
of the cultured mast cells showed that IL-4 increases the expression of
lymphocyte function-associated antigen-1 (LFA-1) and intercellular adhesion
molecule-1 (ICAM-1), but not of very late antigen (VLA) family adhesion
molecules or vascular cell adhesion molecule-1 (VCAM-1). Neutralizing
monoclonal antibodies specific for LFA-1alpha, LFA-1beta, or ICAM-1
inhibited the IL-4-induced homotypic aggregation of the mast cells,
indicating that the aggregation was mediated mainly by LFA-1/ICAM-1
interaction. In addition, IL-4-treated but not untreated mast cells bound
to immobilized ICAM-1. This binding was also inhibited by anti-LFA-1 or
anti-ICAM-1. These results show that IL-4 promotes expression of ICAM-1 and
LFA-1 molecules on mast cells, and suggest that IL-4 may contribute to the
migration of mast cells into the inflamed tissue and to the cellular
interaction with other inflammatory cells by upregulating adhesion
molecules.
Volume 89,
Issue 9,
pp. 3296-3302,
05/01/1997
Copyright © 1997 by The American Society of Hematology
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