Cell recognition molecules play a crucial role in the regulation of immune cells. We recently found that mast cells (MCs) express leukocyte recognition molecules, including ICAM-1 antigen, a natural ligand of LFA-1. We here report that interleukin 4 (IL-4), a pleiotropic cytokine and mast cell differentiation factor, selectively promotes expression of surface ICAM-l antigen and ICAM-1 mRNA in human MCs. IL-4 also up-regulates ICAM-1 antigen in cells of monocyte/macrophage lineage but has no effect on ICAM-1 antigen expressed on basophils, fibroblasts, or lymphocytes. The increase in expression of mast cell/macrophage ICAM-1 antigen induced by IL-4 may contribute to the accumulation of leukocytes and facilitate cell-contact-dependent regulation of immune cells in infammed tissues.Mast cells (MCs) are primarily located in mucosal and perivascular areas of various tissues. They are known to play an important role in allergic events and immune reactions and may accumulate at sites of inflammation together with attracted leukocytes (1). Increasing evidence suggests that cell surface molecules play a significant role in the accumulation, distribution, and regulation of leukocytes in inflammatory reactions (2). We recently found that MCs express leukocyte recognition molecules such as Pgp-1 antigen (CD44) or ICAM-1 antigen (CD54) (3).Interleukin 4 (IL-4) is a pleiotropic immunomodulator active on various cells of hemopoietic origin (4). Previous studies have shown that IL-4 is a differentiation factor for MCs (5,6). We here provide evidence that IL-4, in addition, is involved in the regulation of MC ICAM-1 antigen.MATERIALS AND METHODS Cells. The human mast cell line HMC-1 was established from a patient suffering from MC leukemia (7). Other cell lines used are listed in Table 2. Primary cells were obtained from patients by standard techniques after informed consent was given. MCs were enriched from lung (bronchiogenic carcinoma, n = 4), juvenile foreskin (n = 3), ascitic fluid (n = 4), and gastrointestinal mucosa (n = 2). Lung MC (n = 2) and chronic granulocytic leukemia (CGL) basophils (n = 2) were highly purified (90-98% purity) by negative selection using monoclonal antibodies (mAbs) and complement (8). Mononuclear blood cells (MNCs) were obtained from two normal donors, from two chronic lymphocytic leukemia patients, and from two CGL patients. In addition, tonsillar B cells, cultured umbilical vein endothelial cells, and lung fibroblasts were analyzed. Cells were cultured in complete RPMI medium supplemented with 1o fetal calf serum in a humidified atmosphere of 5% CO2 in air and 37°C.Cytokines. Recombinant human IL-4 (rhIL-4) expressed in Chinese hamster ovary cells was purified by ion-exchange chromatography essentially as described by Widmer et al. (9). Purified rhIL4 had a specific activity of 0.3 x 107 units/mg as defined by the amount of IL-4 required for half-maximal growth of T blasts precultured with 50 ng of rhIL-2 per ml and 1 ,ug of phytohemagglutinin per ml for 5 days. rhIL-2, rhIL-3, rhIL-8, ...

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The syndrome of episodic angioedema and eosinophilia is characterized by cyclic edema, marked peripheral blood eosinophilia, and eosinophil degranulation in the dermis. Using a sensitive immunoenzymetric method, we measured serum interleukin (IL)-5 levels in four patients with this syndrome. We also determined the percentage of activated T cells in the peripheral blood of a new patient before and during an attack. In the patient presented, IL-5 levels peaked several days before maximal eosinophilia and then declined. This patient's lymphocytes showed an increased percentage, 28% (normal 2% to 3%), of activated T cells staining for both CD3 and HLA-DR 10 days before maximal eosinophilia, but no increase at the time of peak eosinophilia. In serum from three previously reported cases, elevated serum IL-5 levels were found during attacks. After glucocorticoid administration, IL-5 levels became undetectable in three of the four patients. Production of IL-5 is likely an important determinant of the pathophysiology of this syndrome.

This study presents the clinical and laboratory findings of a novel syndrome associated with eosinophilia. Two young women presented with marked eosinophilia, and large, non-tender compressible articular nodules arising from the tenosynovium of extensor tendons, dermatitis, episodic swelling of the hands and/or feet and pain in adjacent muscles and joints. Tissue specimens were examined by routine haematoxylin and eosin staining, immunofluorescent staining for eosinophil granule major basic protein (MBP) and rhodamine-avidin or tryptase staining for mast cells. Plasma levels of MBP and eosinophil-derived neurotoxin (EDN) were quantitated by immunoassay. The first patient presented in 1967 at the age of 20 and had, in addition to nodules and eosinophilia, dermographism, recurrent episcleritis and axillary urticaria. Biopsy of a nodule showed tenosynovitis with necrotizing granulomas, non-specific vasculitis, eosinophils and eosinophil degranulation as shown by extracellular deposition of eosinophil granule MBP. Her symptoms responded to low-dose, alternate-day prednisone and have remained quiescent over the past 15 yr. The second patient presented in 1990 at the age of 28 with generalized pruritic dermatitis for 15 yr, eosinophilia for 2 yr, subcutaneous nodules and non-limiting pain in several joints. Biopsy of a nodule showed chronic mild tenosynovitis, numerous eosinophils and extracellular deposition of MBP. She remains untreated. Serum IgE values and plasma levels of MBP and EDN were elevated in both patients; mast cells were numerous in their synovial tissue. Based on their clinical courses, these patients reveal the existence of a distinctive, relatively benign eosinophilic disorder with good long-term prognosis.