Doxycycline induces Fas/Fas ligand-mediated apoptosis in Jurkat T lymphocytes

Jian Liu, Charles A. Kuszynski, Bernard Timothy Baxter

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

Tetracyclines have been used in the treatment of chronic inflammatory diseases associated with local infiltration of inflammatory cells and matrix destruction as observed in rheumatoid arthritis and periodontal disease. Fas/Fas ligand (FasL)-mediated apoptosis plays an important role in maintaining T lymphocyte homeostasis and modulating immune response. The present study demonstrates that doxycycline inhibits Jurkat T lymphocyte proliferation and induces apoptosis. The phytohemagglutinin (PHA)-activated Jurkat cells are more susceptible to doxycycline-induced apoptosis. Furthermore, doxycycline-induced apoptosis is associated with increased Fas/FasL expression in Jurkat cells. The increase of apoptosis in Jurkat cells treated with doxycycline is consistent with the increase of FasL expression. These results suggest that doxycycline may downregulate the inflammatory process in certain diseases by eliminating activated T lymphocytes through Fas/FasL-mediated apoptosis.

Original languageEnglish (US)
Pages (from-to)562-567
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume260
Issue number2
DOIs
StatePublished - Jul 5 1999

Fingerprint

Fas Ligand Protein
T-cells
Doxycycline
Apoptosis
T-Lymphocytes
Jurkat Cells
Tetracyclines
Periodontal Diseases
Phytohemagglutinins
Infiltration
Rheumatoid Arthritis
Homeostasis
Chronic Disease
Down-Regulation

Keywords

  • Apoptosis
  • Cell proliferation
  • Fas
  • Fas ligand
  • T lymphocyte

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Doxycycline induces Fas/Fas ligand-mediated apoptosis in Jurkat T lymphocytes. / Liu, Jian; Kuszynski, Charles A.; Baxter, Bernard Timothy.

In: Biochemical and Biophysical Research Communications, Vol. 260, No. 2, 05.07.1999, p. 562-567.

Research output: Contribution to journalArticle

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