We previously showed that lymphocytes possess the necessary components to constitute an independent, non-neuronal cholinergic system; these include acetylcholine (ACh) itself, choline acetyltransferase (the ACh-synthesizing enzyme), and both muscarinic and nicotinic ACh receptors (AChRs). In addition, we showed that stimulation of AChRs with their respective agonists elicits a variety of biochemical and functional effects, suggesting that lymphocytic cholinergic system is involved in the regulation of immune function. In nerve terminals, choline taken up via the high-affinity choline transporter (CHT1) is exclusively utilized for ACh synthesis. In the present study, therefore, we investigated the expression of CHT1 in T-lymphocytes. Reverse transcription-polymerase chain reaction analysis revealed that MOLT-3 cells, a human leukemic T-cell line used as a T-lymphocyte model, expressed CHT1 mRNA, but that the CEM and Jurkat T-cell lines did not. Consistent with that finding, specific binding of [3H]hemicholinium-3 (HC-3), an inhibitor of CHT1, and HC-3-sensitive [3H]choline uptake were also detected in MOLT-3 cells. These results suggest that CHT1 plays a role in mediating choline uptake in T-lymphocytes and provides further evidence for the presence of an independent lymphocytic cholinergic system.
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