Corticosteroid therapy suppresses spontaneous interleukin 2 release and spontaneous proliferation of lung T lymphocytes of patients with active pulmonary sarcoidosis. Academic Article uri icon

Overview

MeSH

  • Adult
  • Cell Division
  • Depression, Chemical
  • Female
  • Gene Expression Regulation
  • Humans
  • Lymphocyte Activation
  • Male
  • RNA, Messenger
  • Secretory Rate

MeSH Major

  • Adrenal Cortex Hormones
  • Interleukin-2
  • Lung
  • Lung Diseases
  • Sarcoidosis
  • T-Lymphocytes

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 less than 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.

publication date

  • August 1, 1987

has subject area

  • Adrenal Cortex Hormones
  • Adult
  • Cell Division
  • Depression, Chemical
  • Female
  • Gene Expression Regulation
  • Humans
  • Interleukin-2
  • Lung
  • Lung Diseases
  • Lymphocyte Activation
  • Male
  • RNA, Messenger
  • Sarcoidosis
  • Secretory Rate
  • T-Lymphocytes

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed ID

  • 3496388

Additional Document Info

start page

  • 755

end page

  • 760

volume

  • 139

number

  • 3