Spontaneous release of interleukin 2 by lung T lymphocytes in active pulmonary sarcoidosis is primarily from the Leu3+DR+ T cell subset

C. Saltini, J. R. Spurzem, J. J. Lee, P. Pinkston, Ronald Crystal

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Abstract

The inflammation within the lower respiratory tract of individuals with pulmonary sarcoidosis is dominated by large numbers of helper T lymphocytes that proliferate and spontaneously release interleukin 2 (IL-2). To identify the lymphocyte subpopulation that releases IL-2 in this disorder, lung lymphocytes recovered by bronchoalveolar lavage were characterized using the monoclonal antibodies Leu4 (T lymphocyte), Leu 3 (helper/inducer), Leu 2 (suppressor/cytotoxic), and anti-HLA-DR, and separated by panning and flow cytometry. The majority of the IL-2 spontaneously released by T cells in the sarcoid lung was contributed by the Leu3+ cell population (Leu3+ 65 ± 23 IL-2 units released/106 cells per 24 h; Leu2+ 9 ± 8, P<0.04). Further characterization of the lung Leu3+ T cells in sarcoid demonstrated that 30 ± 3% were expressing HLA-DR molecules on their surface compared with 6 ± 1% in normals (P<0.01). Importantly, the subpopulation of Leu3+ lung T lymphocytes expressing a high intensity of HLA-DR molecules on their surface was responsible for the majority of the release of IL-2 in the sarcoid lung (Leu3+ high-intensity DR 42 ± 17 U/106 cells per 24 h, Leu3+ low-intensity DR 8 ± 1 U/106 cells per 24 h; P<0.01). Thus, the spontaneous release of IL-2 in the lung of sarcoid patients appears to be localized to a subset of Leu3+ high-intensity DR ('activated' lung helper/inducer) T lymphocytes. Because the sarcoid lung is characterized by markedly increased numbers of these cells, it is likely that this compartmentalized T cell population plays a major role in sustaining the exaggerated localized immune processes of this disorder.

Original languageEnglish
Pages (from-to)1962-1970
Number of pages9
JournalJournal of Clinical Investigation
Volume77
Issue number6
DOIs
Publication statusPublished - 1 Jan 1986
Externally publishedYes

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Pulmonary Sarcoidosis
T-Lymphocyte Subsets
Interleukin-2
T-Lymphocytes
Lung
HLA-DR Antigens
Helper-Inducer T-Lymphocytes
Immune System Diseases
Lymphocyte Subsets
Bronchoalveolar Lavage
Respiratory System
Population
Flow Cytometry
Cell Count
Monoclonal Antibodies
Lymphocytes
Inflammation

ASJC Scopus subject areas

  • Medicine(all)

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Spontaneous release of interleukin 2 by lung T lymphocytes in active pulmonary sarcoidosis is primarily from the Leu3+DR+ T cell subset. / Saltini, C.; Spurzem, J. R.; Lee, J. J.; Pinkston, P.; Crystal, Ronald.

In: Journal of Clinical Investigation, Vol. 77, No. 6, 01.01.1986, p. 1962-1970.

Research output: Contribution to journalArticle

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title = "Spontaneous release of interleukin 2 by lung T lymphocytes in active pulmonary sarcoidosis is primarily from the Leu3+DR+ T cell subset",
abstract = "The inflammation within the lower respiratory tract of individuals with pulmonary sarcoidosis is dominated by large numbers of helper T lymphocytes that proliferate and spontaneously release interleukin 2 (IL-2). To identify the lymphocyte subpopulation that releases IL-2 in this disorder, lung lymphocytes recovered by bronchoalveolar lavage were characterized using the monoclonal antibodies Leu4 (T lymphocyte), Leu 3 (helper/inducer), Leu 2 (suppressor/cytotoxic), and anti-HLA-DR, and separated by panning and flow cytometry. The majority of the IL-2 spontaneously released by T cells in the sarcoid lung was contributed by the Leu3+ cell population (Leu3+ 65 ± 23 IL-2 units released/106 cells per 24 h; Leu2+ 9 ± 8, P<0.04). Further characterization of the lung Leu3+ T cells in sarcoid demonstrated that 30 ± 3{\%} were expressing HLA-DR molecules on their surface compared with 6 ± 1{\%} in normals (P<0.01). Importantly, the subpopulation of Leu3+ lung T lymphocytes expressing a high intensity of HLA-DR molecules on their surface was responsible for the majority of the release of IL-2 in the sarcoid lung (Leu3+ high-intensity DR 42 ± 17 U/106 cells per 24 h, Leu3+ low-intensity DR 8 ± 1 U/106 cells per 24 h; P<0.01). Thus, the spontaneous release of IL-2 in the lung of sarcoid patients appears to be localized to a subset of Leu3+ high-intensity DR ('activated' lung helper/inducer) T lymphocytes. Because the sarcoid lung is characterized by markedly increased numbers of these cells, it is likely that this compartmentalized T cell population plays a major role in sustaining the exaggerated localized immune processes of this disorder.",
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N2 - The inflammation within the lower respiratory tract of individuals with pulmonary sarcoidosis is dominated by large numbers of helper T lymphocytes that proliferate and spontaneously release interleukin 2 (IL-2). To identify the lymphocyte subpopulation that releases IL-2 in this disorder, lung lymphocytes recovered by bronchoalveolar lavage were characterized using the monoclonal antibodies Leu4 (T lymphocyte), Leu 3 (helper/inducer), Leu 2 (suppressor/cytotoxic), and anti-HLA-DR, and separated by panning and flow cytometry. The majority of the IL-2 spontaneously released by T cells in the sarcoid lung was contributed by the Leu3+ cell population (Leu3+ 65 ± 23 IL-2 units released/106 cells per 24 h; Leu2+ 9 ± 8, P<0.04). Further characterization of the lung Leu3+ T cells in sarcoid demonstrated that 30 ± 3% were expressing HLA-DR molecules on their surface compared with 6 ± 1% in normals (P<0.01). Importantly, the subpopulation of Leu3+ lung T lymphocytes expressing a high intensity of HLA-DR molecules on their surface was responsible for the majority of the release of IL-2 in the sarcoid lung (Leu3+ high-intensity DR 42 ± 17 U/106 cells per 24 h, Leu3+ low-intensity DR 8 ± 1 U/106 cells per 24 h; P<0.01). Thus, the spontaneous release of IL-2 in the lung of sarcoid patients appears to be localized to a subset of Leu3+ high-intensity DR ('activated' lung helper/inducer) T lymphocytes. Because the sarcoid lung is characterized by markedly increased numbers of these cells, it is likely that this compartmentalized T cell population plays a major role in sustaining the exaggerated localized immune processes of this disorder.

AB - The inflammation within the lower respiratory tract of individuals with pulmonary sarcoidosis is dominated by large numbers of helper T lymphocytes that proliferate and spontaneously release interleukin 2 (IL-2). To identify the lymphocyte subpopulation that releases IL-2 in this disorder, lung lymphocytes recovered by bronchoalveolar lavage were characterized using the monoclonal antibodies Leu4 (T lymphocyte), Leu 3 (helper/inducer), Leu 2 (suppressor/cytotoxic), and anti-HLA-DR, and separated by panning and flow cytometry. The majority of the IL-2 spontaneously released by T cells in the sarcoid lung was contributed by the Leu3+ cell population (Leu3+ 65 ± 23 IL-2 units released/106 cells per 24 h; Leu2+ 9 ± 8, P<0.04). Further characterization of the lung Leu3+ T cells in sarcoid demonstrated that 30 ± 3% were expressing HLA-DR molecules on their surface compared with 6 ± 1% in normals (P<0.01). Importantly, the subpopulation of Leu3+ lung T lymphocytes expressing a high intensity of HLA-DR molecules on their surface was responsible for the majority of the release of IL-2 in the sarcoid lung (Leu3+ high-intensity DR 42 ± 17 U/106 cells per 24 h, Leu3+ low-intensity DR 8 ± 1 U/106 cells per 24 h; P<0.01). Thus, the spontaneous release of IL-2 in the lung of sarcoid patients appears to be localized to a subset of Leu3+ high-intensity DR ('activated' lung helper/inducer) T lymphocytes. Because the sarcoid lung is characterized by markedly increased numbers of these cells, it is likely that this compartmentalized T cell population plays a major role in sustaining the exaggerated localized immune processes of this disorder.

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