Human Lymphocyte aggregation?

LAZZARI MA; SCHATTNER M; FINIASZ MR; GIMENO MF

Prostaglandins Leukotrienes and Medicine

Año: 1984 vol. 15 p. 303 - 316

The purpose of the present study was to assess lymphocyte (L) aggregation. Mononuclear cells were obtained according to Boÿum. Blood was defibrinated with glass beads and laid on Ficoll-Hypaque gradients. Monocyte depletion was achieved by adherence to plastic for 18 hs. L aggregation was assayed using the turbidimetric method. When L were challenged with collagen (1-8 micrograms/ml), ADP (2.5 microM), epinephrine (1 X 10(-4) M), ristocetin (1.5 mg/ml) and bovine F VIII no aggregation could be observed. When L were stimulated by arachidonic acid (AA) (160 microM) a complete and irreversible aggregation was obtained. This effect was markedly inhibited when L were previously incubated with aspirin (40 micrograms/ml). On the other hand 5, 8, 11, 14 eicosatetraynoic acid (ETYA), a lypoxygenase inhibitor, was not able to reverse L aggregation induced by AA. Leukotriene B4, C4 and D4 were not able to induce L aggregation. When TXA2 like material from platelets and L was transferred to L preincubated with aspirin a normal aggregation response was obtained. All these results lead to the concept that the main pathway involved in L AA metabolism is probably cyclo-oxygenase. Ionophore A 23187 was not able to induce L aggregation at any concentration employed (0.1 - 100 microM) and 6 keto PGE1 could not inhibit AA induced lymphocyte aggregation.