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Arachidonic acid metabolites in normal and autoimmune mice do not influence lymphocyte‐high endothelial venule interactions
Author(s) -
MANOLIOS N.,
BAKIERA B.,
GECZY C. L.,
SCHRIEBER L.
Publication year - 1991
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.1991.6
Subject(s) - arachidonic acid , lymphocyte , high endothelial venules , immunology , biology , prostaglandin e , chemistry , endocrinology , biochemistry , enzyme
Summary In peripheral lymphoid organs the number of lymphocytes and the proportion of functional lymphocyte subsets are regulated by multiple factors including the control of lymphocyte migration by selective lymphocyte‐high endothelial venule (HEV) interactions. In this study, prostaglandin E 2 (PGE 2 ) levels from normal and autoimmune mouse lymph node cells were measured. The contribution of eicosanoids to lymphocyte‐HEV interactions in normal (CBA/T6) and autoimmune (MRL/n) mice was examined. There was no association between PGE 2 production in normal or autoimmune mice and the age of onset of disease activity in the latter strains. Arachidonic acid metabolites, in particular PGE 2 and leukotriene B 4 (LTB 4 ), did not have any effects on lymphocyte‐HEV binding. Likewise, lymphocytes treated in vivo and/or in vitro with arachidonic acid metabolite inhibitors (acetyl salicylic acid, indomethacin, BW755C) did not alter lymphocyte‐HEV binding interactions in both normal and autoimmune mice. No clinical significance could be attributed to lymph node PGE 2 production and the age of onset of autoimmune disease. In summary, these findings cast doubt on the role of arachidonic acid metabolites in lymphocyte‐HEV binding interactions.