Spontaneous Release of Interleukin-2 by Lung T Lymphocytes in Active Pulmonary Sarcoidosis

Paula Pinkston, Peter B. Bitterman, Ronald Crystal

Research output: Contribution to journalArticle

236 Citations (Scopus)

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<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<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. (N Engl J Med. 1983; 308:793–800.) Sarcoidosis is a chronic multisystem disorder characterized in affected organs by an accumulation of mononuclear inflammatory and immune effector cells, noncaseating granulomas, and derangement of normal tissue architecture.1,2 Although most organs can be affected by this disorder, the lung is most commonly involved and is the site of disease that results in the highest morbidity and mortality.2 The first manifestation of sarcoidosis in the lung is alveolitis, an accumulation of mononuclear effector cells within the alveolar structures.3 The alveolitis in active sarcoidosis is characterized by a marked increase in the number of activated T lymphocytes and, to a lesser degree,.

Original languageEnglish
Pages (from-to)793-800
Number of pages8
JournalNew England Journal of Medicine
Volume308
Issue number14
DOIs
Publication statusPublished - 7 Apr 1983
Externally publishedYes

Fingerprint

Pulmonary Sarcoidosis
Interleukin-2
Sarcoidosis
T-Lymphocytes
Lung
Idiopathic Pulmonary Fibrosis
Alveolar Epithelial Cells
Granuloma
Blood Cells

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Spontaneous Release of Interleukin-2 by Lung T Lymphocytes in Active Pulmonary Sarcoidosis. / Pinkston, Paula; Bitterman, Peter B.; Crystal, Ronald.

In: New England Journal of Medicine, Vol. 308, No. 14, 07.04.1983, p. 793-800.

Research output: Contribution to journalArticle

@article{be558eecbcdb4602923d9ec2d253b30c,
title = "Spontaneous Release of Interleukin-2 by Lung T Lymphocytes in Active Pulmonary Sarcoidosis",
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<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<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. (N Engl J Med. 1983; 308:793–800.) Sarcoidosis is a chronic multisystem disorder characterized in affected organs by an accumulation of mononuclear inflammatory and immune effector cells, noncaseating granulomas, and derangement of normal tissue architecture.1,2 Although most organs can be affected by this disorder, the lung is most commonly involved and is the site of disease that results in the highest morbidity and mortality.2 The first manifestation of sarcoidosis in the lung is alveolitis, an accumulation of mononuclear effector cells within the alveolar structures.3 The alveolitis in active sarcoidosis is characterized by a marked increase in the number of activated T lymphocytes and, to a lesser degree,.",
author = "Paula Pinkston and Bitterman, {Peter B.} and Ronald Crystal",
year = "1983",
month = "4",
day = "7",
doi = "10.1056/NEJM198304073081401",
language = "English",
volume = "308",
pages = "793--800",
journal = "New England Journal of Medicine",
issn = "0028-4793",
publisher = "Massachussetts Medical Society",
number = "14",

}

TY - JOUR

T1 - Spontaneous Release of Interleukin-2 by Lung T Lymphocytes in Active Pulmonary Sarcoidosis

AU - Pinkston, Paula

AU - Bitterman, Peter B.

AU - Crystal, Ronald

PY - 1983/4/7

Y1 - 1983/4/7

N2 - 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<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<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. (N Engl J Med. 1983; 308:793–800.) Sarcoidosis is a chronic multisystem disorder characterized in affected organs by an accumulation of mononuclear inflammatory and immune effector cells, noncaseating granulomas, and derangement of normal tissue architecture.1,2 Although most organs can be affected by this disorder, the lung is most commonly involved and is the site of disease that results in the highest morbidity and mortality.2 The first manifestation of sarcoidosis in the lung is alveolitis, an accumulation of mononuclear effector cells within the alveolar structures.3 The alveolitis in active sarcoidosis is characterized by a marked increase in the number of activated T lymphocytes and, to a lesser degree,.

AB - 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<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<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. (N Engl J Med. 1983; 308:793–800.) Sarcoidosis is a chronic multisystem disorder characterized in affected organs by an accumulation of mononuclear inflammatory and immune effector cells, noncaseating granulomas, and derangement of normal tissue architecture.1,2 Although most organs can be affected by this disorder, the lung is most commonly involved and is the site of disease that results in the highest morbidity and mortality.2 The first manifestation of sarcoidosis in the lung is alveolitis, an accumulation of mononuclear effector cells within the alveolar structures.3 The alveolitis in active sarcoidosis is characterized by a marked increase in the number of activated T lymphocytes and, to a lesser degree,.

UR - http://www.scopus.com/inward/record.url?scp=0020541599&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020541599&partnerID=8YFLogxK

U2 - 10.1056/NEJM198304073081401

DO - 10.1056/NEJM198304073081401

M3 - Article

C2 - 6601235

AN - SCOPUS:0020541599

VL - 308

SP - 793

EP - 800

JO - New England Journal of Medicine

JF - New England Journal of Medicine

SN - 0028-4793

IS - 14

ER -