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Role of interleukin-2 release by lung T-cells in active pulmonary sarcoidosis.
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1983
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Inflammatory Lung DiseaseLung InflammationImmunologyPathologyImmunologic MechanismCd4 T Cell ResponsesInflammationActive Pulmonary SarcoidosisImmunopathologyAutoimmune DiseaseIl-2 PresentPulmonary FibrosisAutoimmunityT Cell ImmunityInterleukin-2 ReleaseLung T-cellsPulmonary SarcoidosisCytokineCellular Immune ResponseMolecular WeightMedicineMatrikines
Using a human T-cell line sensitive to interleukin-2 (IL-2), we evaluated supernatants of unstimulated, purified lung T-lymphocytes from patients with sarcoidosis and high-intensity alveolitis (active disease), patients with sarcoidosis and low-intensity alveolitis (inactive disease), patients with idiopathic pulmonary fibrosis, and normal volunteers for the presence of IL-2. After 24 h in culture, supernatants of lung T-cells from patients with sarcoidosis and high-intensity alveolitis contained significantly greater amounts of IL-2 than did supernatants of lung T-cells from the other 3 groups, which we used as controls (p less than 0.001 for each comparison). The IL-2 present in supernatants of lung T-cells had a molecular weight of approximately 15,000 daltons and the supernatants that contained IL-2 significantly (p less than 0.01) increased in vitro immunoglobulin production by T-cell-depleted normal mononuclear cell suspensions stimulated with pokeweed mitogen. These studies suggest that the release of IL-2 by lung T-cells may explain in part the local proliferation of T-cells and hypergammaglobulinemia that are characteristic of pulmonary sarcoidosis.