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RESEARCH PRODUCT

5-HT3 receptor-channels coupled with Na+ influx in human T cells: role in T cell activation.

Jean-pierre PoissonNaim-akhtar Khan

subject

AgonistSerotoninmedicine.drug_classMetoclopramideT cellT-LymphocytesImmunologyBiologyLymphocyte ActivationJurkat cellsCalcium in biologyPiperazinesSodium ChannelsGranisetronJurkat CellsQuinoxalinesmedicineImmunology and AllergyHumansCalcium SignalingPhytohemagglutininsReceptorProtein kinase C5-HT receptorProtein Kinase C8-Hydroxy-2-(di-n-propylamino)tetralinIon TransportRyanodineCell CycleSodiumCell biologyNeoplasm ProteinsSerotonin Receptor AgonistsEnzyme Activationmedicine.anatomical_structureNeurologyReceptors SerotoninReceptor Serotonin 5-HT1BThapsigarginNeurology (clinical)Serotonin AntagonistsReceptors Serotonin 5-HT3Ion Channel GatingReceptors Serotonin 5-HT1Intracellular

description

The study was conducted on a human (Jurkat) T cell line, loaded with a Na+ fluorescent probe, SBFI/AM. Serotonin and an agonist of 5-HT3 receptor-channels, 2-methyl-5HT, evoked Na+ influx, whereas the agonists of other serotonergic receptor subtypes, i.e., 5-HT1A and 5-HT1B receptors, failed to induce Na+ influx in these cells. By using 3H-BRL43694, an agonist of 5-HT3 receptor-channels, we characterized 5-HT3 lymphocyte receptors which exhibited a density (Bmax) of 300 +/- 20 fmol/10(6) cells and a Kd of 30 nM in Jurkat T cells. The T-cell 5-HT3 receptor-channel is not regulated either by the protein kinase C or by the free intracellular calcium concentrations as the agents known to activate the PKC and to induce increases in intracellular free calcium concentrations failed to influence the free intracellular Na+ concentrations, [Na+]i, in these cells. Furthermore, an increase in [Na+]i, induced by 2-methyl-5HT, via 5-HT3 receptor-channels seems to stimulate T-cell activation by facilitating the progression of T cells from S to G2/M phase of the cell cycle.

10.1016/s0165-5728(99)00101-0https://pubmed.ncbi.nlm.nih.gov/10496177