Regulation of human B cell proliferation by prostaglandin E2

P. A. Thompson, D. F. Jelinek, P. E. Lipsky

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59 Scopus citations

Abstract

The role of prostaglandin E2 (PGE2) in the regulation of human B cell proliferation in vitro was examined. Initial studies demonstrated that monocyte (Mφ)-mediated suppression of B cell proliferation in Staphylococcus aureus (SA)-stimulated cultures was diminished by indomethacin, and thus it was suggested that cyclooxygenase pathway products of arachidonic acid played a role in the regulation of B cell activation. The possibility that PGE2, one of the major products of this pathway generated by Mφ, affected human B cell responses was therefore investigated. PGE2 was found to suppress B cell DNA synthesis and proliferation stimulated by SA in the presence or absence of B cell growth factor (BCGF)-containing T cell supernatants. Suppression was concentration-dependent; significant inhibition was observed in indomethacin-blocked cultures with 10-10 to 10-9 M PGE2. In contrast to the effect of PGE2 on SA-induced B cell proliferation, it had minimal effect on pokeweed mitogen (PWM)-stimulated B cell or T cell DNA synthesis. The effect of PGE2 on the generation of BCGF activity from mitogen-stimulated T cells was also examined. PGE2 (10-7 M) did not inhibit the production of BCGF activity from PWM-stimulated T cells, or from T cells stimulated with the combination of phytohemagglutinin and phorbol myristate acetate. Thus, PGE2 inhibits B cell proliferation in response to SA but not PWM, and has little effect on the production of BCGF by T cells. These results indicate that PGE2 at physiologically relevant concentrations exerts selective regulatory effects on human B cell responses.

Original languageEnglish (US)
Pages (from-to)2446-2453
Number of pages8
JournalJournal of Immunology
Volume133
Issue number5
StatePublished - Dec 1 1984

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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