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CD4⁺ T Cell and Eosinophil Adhesion Is Mediated by Specific ICAM-3 Ligation and Results in Eosinophil Activation¹

Section of Pulmonary and Critical Care Medicine, Department of Medicine, and Departments of Pharmacological and Physiological Sciences, Pediatrics, Anesthesia, and Critical Care, and Committees on Clinical Pharmacology, Cell Physiology, and Immunology, Division of Biological Sciences, University of Chicago, Chicago, IL 60637

T cells and eosinophils, which are found in close proximity in asthmatic lungs, express many surface receptors that are counterligands. These data suggest that direct interactions between these cell types could play an important role in regulating airway inflammation in asthma. We examined the effect of selective adhesion between counterligands on human eosinophils and CD4⁺ T cells to determine 1) the existence of specific adhesive interactions and 2) if augmented specific adhesion to CD4⁺ T cells also caused augmented secretion of leukotriene C₄ (LTC₄) from eosinophils. A new method for binding of human CD4⁺ T cells to microwell plates was developed, which allowed for specific quantitative assessment of eosinophil adhesion to individual CD4⁺ T cells in culture. Adhesion of CD4⁺ T cells to eosinophils was minimal in unstimulated cells but increased after activation of T cells by PMA. Augmented adhesion was regulated substantially through binding of ICAM-3 and only minimally by ICAM-1. We further evaluated whether this specific adhesion up-regulated stimulated secretion of LTC₄ from eosinophils. Adhesion with CD4⁺ T cells augmented eosinophil secretion of LTC₄ caused by FMLP plus cytochalasin. Blockade of ICAM-3, as well as ICAM-1, inhibited completely the augmented secretion of eosinophil LTC₄. We demonstrate that eosinophils and CD4⁺ T cells are capable of ligand-specific adhesion that is mediated predominantly by ICAM-3 ligation and that this binding causes augmented eosinophil secretion.

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