Spontaneous release of interleukin-2 by lung T lymphocytes in active pulmonary sarcoidosis.
| Publication Type | Academic Article |
| Authors | Pinkston P, Bitterman P, Crystal R |
| Journal | N Engl J Med |
| Volume | 308 |
| Issue | 14 |
| Pagination | 793-800 |
| Date Published | 04/07/1983 |
| ISSN | 0028-4793 |
| Keywords | Interleukin-2, Lung, Lung Diseases, Sarcoidosis, T-Lymphocytes |
| Abstract | We investigated the possible role of interleukin-2, a T-cell product that stimulates the clonal increase of responsive T lymphocytes, in the pathogenesis of pulmonary sarcoidosis. We obtained mononuclear effector cells from the lungs of 10 patients with sarcoidosis and high-intensity alveolitis, 17 patients with sarcoidosis and low-intensity alveolitis, 3 patients with idiopathic pulmonary fibrosis, and 10 normal controls. Lung cells from the group with sarcoidosis and low-intensity alveolitis, from the group with idiopathic pulmonary fibrosis, and from the controls produced insignificant amounts of interleukin-2. However, lung cells from 9 of 10 patients with sarcoidosis and high-intensity alveolitis spontaneously released interleukin-2, and in a proportion that correlated with the proportion of T cells in the lung washings (P less than 0.01). Blood T cells from the same patients did not release interleukin-2. To determine whether release of interleukin-2 by the lung T cells had a biologic effect in vivo, we measured T-lymphocyte replication in the lungs of patients and controls. The lung T lymphocytes replicated at a rate that was several times higher in the patients with sarcoidosis and high-intensity alveolitis than in the other patient groups or the controls (P less than 0.01). These observations suggest that the release of interleukin-2 by lung T cells has a central role in increasing the numbers of lung T cells in active pulmonary sarcoidosis. |
| DOI | 10.1056/NEJM198304073081401 |
| PubMed ID | 6601235 |