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Regulation of T-lymphopoiesis by arachidonic acid metabolites.

Abstract：

:The cloning efficiency of T-lymphocyte progenitor cells (CFU-T) is dependent on mononuclear cell concentration, with a triphasic growth curve. At low plating cell concentrations, hydrocortisone causes a dose-dependent decrease in cloning efficiency, whereas at high cell concentrations hydrocortisone causes increased cloning efficiency. To determine if the biphasic effects of hydrocortisone are through its inhibition of arachidonic acid metabolism, we tested the effects of various arachidonic acid metabolism inhibitors on cloning efficiency. Indomethacin, which inhibits cyclooxygenase, has no effect at low cell plating doses, but increases cloning efficiency at high cell doses. Prostaglandin E2 (PGE2) causes a dose-dependent inhibition of cloning efficiency at all cell doses. Caffeic acid, an inhibitor of lipoxygenase, causes a dose-dependent inhibition of CFU-T, particularly at lower cell concentrations. Leukotriene B4 (LTB4) restored caffeic acid-inhibited growth, as did addition of recombinant interleukins 1 and 2 (IL-1 and IL-2). These results support a regulatory role for arachidonic acid metabolites in T-lymphopoiesis. PGE2, a cyclooxygenase product, is inhibitory, whereas LTB4, a lipoxygenase product, is stimulatory through its role in IL-1 synthesis.

journal_name

Exp Hematol

journal_title

Experimental hematology

authors

Miller AM,Elfenbein GJ,Barth KC

subject

Has Abstract

pub_date

1989-02-01 00:00:00

pages

198-202

issue

2

eissn

0301-472X

issn

1873-2399

journal_volume

17

pub_type

杂志文章

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