Effects of arachidonic acid metabolites and other compounds on the CTLL assay for interleukin-2

Mark K. Eskandari, Steven L. Kunkel, Daniel G. Remick*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Interleukin-2 (IL-2) is a peptide lymphokine which plays a central role in many immune responses. Production of IL-2 is blocked in the presence of various chemical constituents including arachidonic acid (AA) metabolites, however, the effects of these compounds on preformed IL-2 is less clear. This study was designed to observe whether commonly employed drugs and AA metabolites will inhibit the ability to measure IL-2 in a standard bioassay. We measured cytotoxic T lymphocyte (CTLL) proliferation in response to IL-2 in the presence of increasing concentrations of drugs or AA metabolites. Our data provides clear evidence that no suppression of cell replication occurs with PGE2, PGF, LTB4, LTC4, LTD4, and LTE4 at concentrations of 10-5-10-9 M. At high concentrations, both dexamethasone (10-5 M) and indomethacin (10-5 and 10-6 M) resulted in a suppressive effect on CTLL proliferation, while low concentrations of either compound (10-7-10-9 M) had no effect. This study shows that AA metabolites will not block the ability of IL-2 to induce CTLL proliferation, and neither will dexamethasone or indomethacin at low concentrations.

Original languageEnglish (US)
Pages (from-to)85-89
Number of pages5
JournalJournal of Immunological Methods
Volume118
Issue number1
DOIs
StatePublished - Mar 10 1989

Keywords

  • Arachidonic acid metabolite
  • Interleukin-2
  • Prostaglandin

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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