Corticosteroid therapy suppresses spontaneous interleukin 2 release and spontaneous proliferation of lung T lymphocytes of patients with active pulmonary sarcoidosis

P. Pinkston, C. Saltini, J. Muller-Quernheim, Ronald Crystal

Research output: Contribution to journalArticle

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Abstract

Active pulmonary sarcoidosis is characterized by the alveolar accumulation of activated helper T lymphocytes that are spontaneously releasing IL 2 and proliferating at an enhanced rate. In this regard, sarcoidosis represents a 'model' human disorder to test in vivo the known in vitro action of corticosteroids on suppressing the activated IL 2 gene. Comparable groups of patients with active sarcoidosis were prospectively evaluated with no therapy or treated with corticosteroids. Over 3.2 ± 0.4 mo, the untreated group had no significant change in spontaneous lung T cell release of IL 2 or spontaneous proliferation. In contrast, over the same period, the treated group had marked reduction of spontaneous lung T cell release of IL 2 and proliferation (p < 0.01, all comparisons before therapy). Furthermore, Northern analysis of lung T cell RNA before therapy demonstrated IL 2 mRNA transcripts, whereas no IL 2 transcripts were observed during therapy. These observations are consistent with the concept that directly, or indirectly, corticosteroids are capable of suppressing the IL 2 gene in activated T lymphocytes in vivo.

Original languageEnglish
Pages (from-to)755-760
Number of pages6
JournalJournal of Immunology
Volume139
Issue number3
Publication statusPublished - 1 Jan 1987
Externally publishedYes

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Pulmonary Sarcoidosis
Interleukin-2
Adrenal Cortex Hormones
T-Lymphocytes
Lung
Sarcoidosis
Therapeutics
Helper-Inducer T-Lymphocytes
Genes
RNA
Messenger RNA

ASJC Scopus subject areas

  • Immunology

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Corticosteroid therapy suppresses spontaneous interleukin 2 release and spontaneous proliferation of lung T lymphocytes of patients with active pulmonary sarcoidosis. / Pinkston, P.; Saltini, C.; Muller-Quernheim, J.; Crystal, Ronald.

In: Journal of Immunology, Vol. 139, No. 3, 01.01.1987, p. 755-760.

Research output: Contribution to journalArticle

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