Danazol suppresses both spontaneous and activated human lymphocyte- mediated cytotoxicity

P. Vigano, A. M. Di Blasio, M. Busacca, M. G. Sabbadini, M. Vignali

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Danazol is an effective drug in the treatment of endometriosis. Previous reports suggest that it can act by influencing the immune system. Thus, in this study we evaluated whether danazol is able to affect the expression of natural and activated cytotoxicity by human peripheral blood lymphocytes (PBL). A cytotoxicity assay by 51Cr release was performed to determine the effect of danazol on lymphocyte cytotoxic response toward an erytroleukemic cell line (K562). A significant suppression of spontaneous cytotoxicity was observed when lymphocytes were pretreated for 18 h with danazol at the concentration of 5 x 10-6 M. In addition, danazol could significantly inhibit both IL-2- and INFα-activated cytotoxicity at the concentration of 10-5 M. Following 18 h exposure to danazol, PBL were able to completely recover their spontaneous but not activated cytotoxic potential upon further in vitro incubation (18 h) in absence of the drug. The biological significance of danazol as an inhibitor of immune function under experimentally defined conditions is discussed in relation to its possible role in vivo.

Original languageEnglish
Pages (from-to)38-42
Number of pages5
JournalAmerican Journal of Reproductive Immunology
Volume28
Issue number1
Publication statusPublished - 1992

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Danazol
Lymphocytes
Endometriosis
Pharmaceutical Preparations
Interleukin-2
Immune System
Cell Line

Keywords

  • Danazol
  • interferon α
  • interleukin-2
  • natural killers

ASJC Scopus subject areas

  • Immunology
  • Obstetrics and Gynaecology

Cite this

Danazol suppresses both spontaneous and activated human lymphocyte- mediated cytotoxicity. / Vigano, P.; Di Blasio, A. M.; Busacca, M.; Sabbadini, M. G.; Vignali, M.

In: American Journal of Reproductive Immunology, Vol. 28, No. 1, 1992, p. 38-42.

Research output: Contribution to journalArticle

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