GASTRIN-CCK-B TYPE RECEPTORS ON HUMAN T-LYMPHOBLASTOID JURKAT CELLS

The presence of specific receptors for gastrointestinal hormones on T cells and their involvement in the immune response are still matters o f debate. We reported the effects of gastrin cholecystokinin (CCK)-rel ated peptides on J.RT3-T3.5 Jurkat cells. A single class of high-affin ity binding sites (dissociation constant similar to 0.1 nM) for gastri n and CCK-8 was evident on these cells. These peptides dose-dependentl y induced a transient increase in intracellular Ca2+ concentration ([C a2+](i)), which was independent of extracellular Ca2+. L-365,260 was 1 50- to 300-fold more potent than L-364,718 to inhibit radiola- beled l igand binding or peptide-stimulated [Ca2+](i) increase, confirming the gastrin-CCK-B nature of the receptor. Gastrin caused a rise in inosit ol 1,4,5-trisphosphate [Ins(1,4,5)P-3] level within 5 s of stimulation . Finally, gastrin increased interleukin (IL)-2 secretion in J.RT3-T3. 5 cells. We concluded that 1) J.RT3-T3.5 cells possess ''gastrin-CCK-B type'' receptors coupled to phospholipase C activation, Ins(1,4,5)P-3 formation, and Ca2+ release from intracellular Ca2+ pools, and 2) the se receptors could be involved in the regulation of IL-2 production.