Effect of interstitial lung disease macrophages on T-cell signal transduction

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Some types of interstitial lung disease (ILD) are characterized by an abnormal proliferation and activation of lymphocytes in the alveolus and interstitium. Recent data have suggested that membrane signals on alveolar macrophages (AM) in normal lung play a crucial role in limiting lymphocyte activation by altering early events in receptor-mediated signal transduction in lymphocytes. In the current study fixed AM from normal volunteers and from patients with either sarcoidosis or idiopathic pulmonary fibrosis were compared for the ability to inhibit CD3-mediated increases in intracellular calcium concentration [(Ca2+)i]. All normal AM inhibited CD3-mediated increases in (Ca2+)i, whereas seven of 10 ILD AM were permissive of this early event in T-lymphocyte activation. Patients with ILD and permissive AM displayed significantly greater mean BAL lymphocytes than did those with suppressive AM (42 versus 12%, respectively). The inhibitory effect of normal AM could be partially duplicated by incubation of lymphocytes with surfactant (SF) obtained from normal lungs. Analysis of one SF component, SF protein A, in normal and in ILD AM membranes disclosed reduced SF protein A in ILD AM. These results demonstrate alterations in AM in patients with ILD and a lymphocytic alveolitis that renders AM permissive for early events in T-cell activation.

Original languageEnglish (US)
Pages (from-to)191-196
Number of pages6
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume149
Issue number1
StatePublished - Jan 1994

Fingerprint

Interstitial Lung Diseases
Alveolar Macrophages
Signal Transduction
Macrophages
T-Lymphocytes
Lymphocyte Activation
Pulmonary Surfactant-Associated Protein A
Lymphocytes
Surface-Active Agents
Dimercaprol
Lung
Idiopathic Pulmonary Fibrosis
Membranes
Sarcoidosis
Healthy Volunteers
Calcium

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

@article{abfcfb5775fa457abe8071edf84e5c0b,
title = "Effect of interstitial lung disease macrophages on T-cell signal transduction",
abstract = "Some types of interstitial lung disease (ILD) are characterized by an abnormal proliferation and activation of lymphocytes in the alveolus and interstitium. Recent data have suggested that membrane signals on alveolar macrophages (AM) in normal lung play a crucial role in limiting lymphocyte activation by altering early events in receptor-mediated signal transduction in lymphocytes. In the current study fixed AM from normal volunteers and from patients with either sarcoidosis or idiopathic pulmonary fibrosis were compared for the ability to inhibit CD3-mediated increases in intracellular calcium concentration [(Ca2+)i]. All normal AM inhibited CD3-mediated increases in (Ca2+)i, whereas seven of 10 ILD AM were permissive of this early event in T-lymphocyte activation. Patients with ILD and permissive AM displayed significantly greater mean BAL lymphocytes than did those with suppressive AM (42 versus 12{\%}, respectively). The inhibitory effect of normal AM could be partially duplicated by incubation of lymphocytes with surfactant (SF) obtained from normal lungs. Analysis of one SF component, SF protein A, in normal and in ILD AM membranes disclosed reduced SF protein A in ILD AM. These results demonstrate alterations in AM in patients with ILD and a lymphocytic alveolitis that renders AM permissive for early events in T-cell activation.",
author = "Weissler, {Jonathan C.} and Carole Mendelson and Fernando Moya and Yarbrough, {William C.}",
year = "1994",
month = "1",
language = "English (US)",
volume = "149",
pages = "191--196",
journal = "American Journal of Respiratory and Critical Care Medicine",
issn = "1073-449X",
publisher = "American Thoracic Society",
number = "1",

}

TY - JOUR

T1 - Effect of interstitial lung disease macrophages on T-cell signal transduction

AU - Weissler, Jonathan C.

AU - Mendelson, Carole

AU - Moya, Fernando

AU - Yarbrough, William C.

PY - 1994/1

Y1 - 1994/1

N2 - Some types of interstitial lung disease (ILD) are characterized by an abnormal proliferation and activation of lymphocytes in the alveolus and interstitium. Recent data have suggested that membrane signals on alveolar macrophages (AM) in normal lung play a crucial role in limiting lymphocyte activation by altering early events in receptor-mediated signal transduction in lymphocytes. In the current study fixed AM from normal volunteers and from patients with either sarcoidosis or idiopathic pulmonary fibrosis were compared for the ability to inhibit CD3-mediated increases in intracellular calcium concentration [(Ca2+)i]. All normal AM inhibited CD3-mediated increases in (Ca2+)i, whereas seven of 10 ILD AM were permissive of this early event in T-lymphocyte activation. Patients with ILD and permissive AM displayed significantly greater mean BAL lymphocytes than did those with suppressive AM (42 versus 12%, respectively). The inhibitory effect of normal AM could be partially duplicated by incubation of lymphocytes with surfactant (SF) obtained from normal lungs. Analysis of one SF component, SF protein A, in normal and in ILD AM membranes disclosed reduced SF protein A in ILD AM. These results demonstrate alterations in AM in patients with ILD and a lymphocytic alveolitis that renders AM permissive for early events in T-cell activation.

AB - Some types of interstitial lung disease (ILD) are characterized by an abnormal proliferation and activation of lymphocytes in the alveolus and interstitium. Recent data have suggested that membrane signals on alveolar macrophages (AM) in normal lung play a crucial role in limiting lymphocyte activation by altering early events in receptor-mediated signal transduction in lymphocytes. In the current study fixed AM from normal volunteers and from patients with either sarcoidosis or idiopathic pulmonary fibrosis were compared for the ability to inhibit CD3-mediated increases in intracellular calcium concentration [(Ca2+)i]. All normal AM inhibited CD3-mediated increases in (Ca2+)i, whereas seven of 10 ILD AM were permissive of this early event in T-lymphocyte activation. Patients with ILD and permissive AM displayed significantly greater mean BAL lymphocytes than did those with suppressive AM (42 versus 12%, respectively). The inhibitory effect of normal AM could be partially duplicated by incubation of lymphocytes with surfactant (SF) obtained from normal lungs. Analysis of one SF component, SF protein A, in normal and in ILD AM membranes disclosed reduced SF protein A in ILD AM. These results demonstrate alterations in AM in patients with ILD and a lymphocytic alveolitis that renders AM permissive for early events in T-cell activation.

UR - http://www.scopus.com/inward/record.url?scp=0028085029&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028085029&partnerID=8YFLogxK

M3 - Article

VL - 149

SP - 191

EP - 196

JO - American Journal of Respiratory and Critical Care Medicine

JF - American Journal of Respiratory and Critical Care Medicine

SN - 1073-449X

IS - 1

ER -