Characterization of mononuclear phagocyte subpopulations in the human lung by using monoclonal antibodies: Changes in alveolar macrophage phenotype associated with pulmonary sarcoidosis

A. J. Hance, S. Douches, R. J. Winchester, V. J. Ferrans, Ronald Crystal

Research output: Contribution to journalArticle

86 Citations (Scopus)

Abstract

Current concepts of pulmonary sarcoidosis suggest that the alveolar macrophage plays a central role in the pathogenesis of the disease. To help define the population of alveolar macrophages in sarcoidosis, we compared the surface phenotype of alveolar macrophages from patients with sarcoidosis and from normal individuals by using monoclonal antibodies (63D3, OKM1, MΦP-9, MΦS-1, 61D3, and MΦS-39) that detect surface antigens on cells of monocyte/macrophage lineage. Although almost all blood monocytes expressed surface antigens detected by each of these antibodies, only a minority of normal alveolar macrophages expressed the same surface antigens (p < 0.05, each comparison). However, in sarcoidosis, the percentage of alveolar macrophages expressing these surface antigens was increased (p < 0.05, each comparison with normal alveolar macrophages). Several findings supported the conclusion that the increasd expression of these monocyte-linkage surface antigens on sarcoid alveolar macrophages resulted from increased recruitment of monocytes to the lung in sarcoidosis and not from abnormal 'activation' of alveolar macrophages. First, alveolar macrophages expressing these antigens had an immature morphology. Second, in vitro cultivation of blood monocytes and alveolar macrophages in the presence of immune and inflammatory mediators, including mediators known to be present in the lung in sarcoidosis, did not prevent the loss of expression of monocyte-lineage surface antigens from monocytes or induce reexpression of monocyte-lineage surface antigens on alveolar macrophages. Third, the expression of monocyte-lineage surface antigens was only increased on sarcoid macrophages from patients whose lower respiratory tract contained an increased number of T lymphocytes, cells known to release monocyte chemotactic factor in sarcoidosis. Consistent with the knowledge that corticosteroids usually suppress the alveolitis of active sarcoidosis, when the expression of alveolar macrophage surface antigens was evaluated before and during therapy, the percentage of alveolar macrophage expressing monocyte-lineage surface antigens returned to normal after 1 to 3 mo of therapy. These observations support the concept that the changes in the alveolar macrophage population in sarcoidosis are linked, at least in part, to increased recruitment of blood monocytes to the lung and suggest that the population of alveolar macrophages in sarcoidosis is relatively immature compared with the alveolar macrophages present in the normal lung.

Original languageEnglish
Pages (from-to)284-292
Number of pages9
JournalJournal of Immunology
Volume134
Issue number1
Publication statusPublished - 6 Mar 1985
Externally publishedYes

Fingerprint

Pulmonary Sarcoidosis
Alveolar Macrophages
Phagocytes
Monoclonal Antibodies
Phenotype
Surface Antigens
Monocytes
Lung
Sarcoidosis
Macrophages
Population
Chemotactic Factors

ASJC Scopus subject areas

  • Immunology

Cite this

Characterization of mononuclear phagocyte subpopulations in the human lung by using monoclonal antibodies : Changes in alveolar macrophage phenotype associated with pulmonary sarcoidosis. / Hance, A. J.; Douches, S.; Winchester, R. J.; Ferrans, V. J.; Crystal, Ronald.

In: Journal of Immunology, Vol. 134, No. 1, 06.03.1985, p. 284-292.

Research output: Contribution to journalArticle

@article{9c9d08dec29446c4b34baca074db3520,
title = "Characterization of mononuclear phagocyte subpopulations in the human lung by using monoclonal antibodies: Changes in alveolar macrophage phenotype associated with pulmonary sarcoidosis",
abstract = "Current concepts of pulmonary sarcoidosis suggest that the alveolar macrophage plays a central role in the pathogenesis of the disease. To help define the population of alveolar macrophages in sarcoidosis, we compared the surface phenotype of alveolar macrophages from patients with sarcoidosis and from normal individuals by using monoclonal antibodies (63D3, OKM1, MΦP-9, MΦS-1, 61D3, and MΦS-39) that detect surface antigens on cells of monocyte/macrophage lineage. Although almost all blood monocytes expressed surface antigens detected by each of these antibodies, only a minority of normal alveolar macrophages expressed the same surface antigens (p < 0.05, each comparison). However, in sarcoidosis, the percentage of alveolar macrophages expressing these surface antigens was increased (p < 0.05, each comparison with normal alveolar macrophages). Several findings supported the conclusion that the increasd expression of these monocyte-linkage surface antigens on sarcoid alveolar macrophages resulted from increased recruitment of monocytes to the lung in sarcoidosis and not from abnormal 'activation' of alveolar macrophages. First, alveolar macrophages expressing these antigens had an immature morphology. Second, in vitro cultivation of blood monocytes and alveolar macrophages in the presence of immune and inflammatory mediators, including mediators known to be present in the lung in sarcoidosis, did not prevent the loss of expression of monocyte-lineage surface antigens from monocytes or induce reexpression of monocyte-lineage surface antigens on alveolar macrophages. Third, the expression of monocyte-lineage surface antigens was only increased on sarcoid macrophages from patients whose lower respiratory tract contained an increased number of T lymphocytes, cells known to release monocyte chemotactic factor in sarcoidosis. Consistent with the knowledge that corticosteroids usually suppress the alveolitis of active sarcoidosis, when the expression of alveolar macrophage surface antigens was evaluated before and during therapy, the percentage of alveolar macrophage expressing monocyte-lineage surface antigens returned to normal after 1 to 3 mo of therapy. These observations support the concept that the changes in the alveolar macrophage population in sarcoidosis are linked, at least in part, to increased recruitment of blood monocytes to the lung and suggest that the population of alveolar macrophages in sarcoidosis is relatively immature compared with the alveolar macrophages present in the normal lung.",
author = "Hance, {A. J.} and S. Douches and Winchester, {R. J.} and Ferrans, {V. J.} and Ronald Crystal",
year = "1985",
month = "3",
day = "6",
language = "English",
volume = "134",
pages = "284--292",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "1",

}

TY - JOUR

T1 - Characterization of mononuclear phagocyte subpopulations in the human lung by using monoclonal antibodies

T2 - Changes in alveolar macrophage phenotype associated with pulmonary sarcoidosis

AU - Hance, A. J.

AU - Douches, S.

AU - Winchester, R. J.

AU - Ferrans, V. J.

AU - Crystal, Ronald

PY - 1985/3/6

Y1 - 1985/3/6

N2 - Current concepts of pulmonary sarcoidosis suggest that the alveolar macrophage plays a central role in the pathogenesis of the disease. To help define the population of alveolar macrophages in sarcoidosis, we compared the surface phenotype of alveolar macrophages from patients with sarcoidosis and from normal individuals by using monoclonal antibodies (63D3, OKM1, MΦP-9, MΦS-1, 61D3, and MΦS-39) that detect surface antigens on cells of monocyte/macrophage lineage. Although almost all blood monocytes expressed surface antigens detected by each of these antibodies, only a minority of normal alveolar macrophages expressed the same surface antigens (p < 0.05, each comparison). However, in sarcoidosis, the percentage of alveolar macrophages expressing these surface antigens was increased (p < 0.05, each comparison with normal alveolar macrophages). Several findings supported the conclusion that the increasd expression of these monocyte-linkage surface antigens on sarcoid alveolar macrophages resulted from increased recruitment of monocytes to the lung in sarcoidosis and not from abnormal 'activation' of alveolar macrophages. First, alveolar macrophages expressing these antigens had an immature morphology. Second, in vitro cultivation of blood monocytes and alveolar macrophages in the presence of immune and inflammatory mediators, including mediators known to be present in the lung in sarcoidosis, did not prevent the loss of expression of monocyte-lineage surface antigens from monocytes or induce reexpression of monocyte-lineage surface antigens on alveolar macrophages. Third, the expression of monocyte-lineage surface antigens was only increased on sarcoid macrophages from patients whose lower respiratory tract contained an increased number of T lymphocytes, cells known to release monocyte chemotactic factor in sarcoidosis. Consistent with the knowledge that corticosteroids usually suppress the alveolitis of active sarcoidosis, when the expression of alveolar macrophage surface antigens was evaluated before and during therapy, the percentage of alveolar macrophage expressing monocyte-lineage surface antigens returned to normal after 1 to 3 mo of therapy. These observations support the concept that the changes in the alveolar macrophage population in sarcoidosis are linked, at least in part, to increased recruitment of blood monocytes to the lung and suggest that the population of alveolar macrophages in sarcoidosis is relatively immature compared with the alveolar macrophages present in the normal lung.

AB - Current concepts of pulmonary sarcoidosis suggest that the alveolar macrophage plays a central role in the pathogenesis of the disease. To help define the population of alveolar macrophages in sarcoidosis, we compared the surface phenotype of alveolar macrophages from patients with sarcoidosis and from normal individuals by using monoclonal antibodies (63D3, OKM1, MΦP-9, MΦS-1, 61D3, and MΦS-39) that detect surface antigens on cells of monocyte/macrophage lineage. Although almost all blood monocytes expressed surface antigens detected by each of these antibodies, only a minority of normal alveolar macrophages expressed the same surface antigens (p < 0.05, each comparison). However, in sarcoidosis, the percentage of alveolar macrophages expressing these surface antigens was increased (p < 0.05, each comparison with normal alveolar macrophages). Several findings supported the conclusion that the increasd expression of these monocyte-linkage surface antigens on sarcoid alveolar macrophages resulted from increased recruitment of monocytes to the lung in sarcoidosis and not from abnormal 'activation' of alveolar macrophages. First, alveolar macrophages expressing these antigens had an immature morphology. Second, in vitro cultivation of blood monocytes and alveolar macrophages in the presence of immune and inflammatory mediators, including mediators known to be present in the lung in sarcoidosis, did not prevent the loss of expression of monocyte-lineage surface antigens from monocytes or induce reexpression of monocyte-lineage surface antigens on alveolar macrophages. Third, the expression of monocyte-lineage surface antigens was only increased on sarcoid macrophages from patients whose lower respiratory tract contained an increased number of T lymphocytes, cells known to release monocyte chemotactic factor in sarcoidosis. Consistent with the knowledge that corticosteroids usually suppress the alveolitis of active sarcoidosis, when the expression of alveolar macrophage surface antigens was evaluated before and during therapy, the percentage of alveolar macrophage expressing monocyte-lineage surface antigens returned to normal after 1 to 3 mo of therapy. These observations support the concept that the changes in the alveolar macrophage population in sarcoidosis are linked, at least in part, to increased recruitment of blood monocytes to the lung and suggest that the population of alveolar macrophages in sarcoidosis is relatively immature compared with the alveolar macrophages present in the normal lung.

UR - http://www.scopus.com/inward/record.url?scp=0022006197&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022006197&partnerID=8YFLogxK

M3 - Article

C2 - 3964815

AN - SCOPUS:0022006197

VL - 134

SP - 284

EP - 292

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 1

ER -