Interleukin-4 induces homotypic aggregation of human mast cells by promoting LFA-1/ ICAM-1 adhesion molecules

We report here that interleukin-4 (IL-4) induces homotypic clonal antibodies specific for LFA-1a, LFA-1b, or ICAM-1 in-aggregation of cultured human mast cells, grown from cord hibited the IL-4–induced homotypic aggregation of the mast blood mononuclear cells in the presence of stem cell factor cells, indicating that the aggregation was mediated mainly and IL-6. This aggregation was specifically induced by IL-4, by LFA-1/ICAM-1 interaction. In addition, IL-4–treated but because other cytokines including IL-1a, IL-1b, IL-2, IL-3, IL- not untreated mast cells bound to immobilized ICAM-1. This 5, IL-9, IL-10, interferon-g, IL-12, granulocyte-macrophage binding was also inhibited by anti-LFA-1 or anti-ICAM-1. colony-stimulating factor, NGF-b, and tumor necrosis factor- These results show that IL-4 promotes expression of ICAM-a failed to show such effect. Flow cytometric analysis of the 1 and LFA-1 molecules on mast cells, and suggest that IL-4 cultured mast cells showed that IL-4 increases the expres- may contribute to the migration of mast cells into the in-sion of lymphocyte function-associated antigen-1 (LFA-1) flamed tissue and to the cellular interaction with other in-and intercellular adhesion molecule-1 (ICAM-1), but not of flammatory cells by upregulating adhesion molecules. very late antigen (VLA) family adhesion molecules or vascu-q 1997 by The American Society of Hematology. lar cell adhesion molecule-1 (VCAM-1). Neutralizing mono-A The expression and regulation of adhesion molecules onDHESION MOLECULES on mast cells are believedto be involved in the tissue distribution of mast cells. mast cells has been investigated in the murine system usin