Abstract
A contribution of the cholinergic system to immune cell function has been suggested, though the role of nicotine and its receptors in T cells, especially regulatory T (Treg) cells, is unclear. We herein investigated the expression and function of nicotinic acetylcholine receptors (nAChRs) in murine-induced Treg (iTreg) cells. Upon differentiation of naive BALB/c T cells into iTreg cells and other T-cell subsets, the effect of nicotine on cytokine production and proliferation of iTreg cells was examined. The expression of nAChRs and its regulatory mechanisms were comparatively analyzed among T-cell subsets. Stimulation-induced transforming growth factor-β1 (TGF-β1) production of iTreg cells was suppressed by nicotine, whereas interleukin (IL)-10 production and proliferation was not affected. α2-, α5-, α9-, and β2-nAChRs were differentially expressed in naive, Th1, Th2, Th9, Th17, and iTreg cells. Among these cell types, the α9-nAChR was particularly upregulated in iTreg cells via its gene promoter, but not through tri-methylation at the 4th lysine residue of the histone H3-dependent mechanisms. We conclude that the immunoregulatory role of Treg cells is modified by the cholinergic system, probably through the characteristic expression of nAChRs.
Highlights
Academic Editor: Toshio TakahashiCholinergic neurotransmitters and their corresponding nicotinic acetylcholine receptors play pivotal roles in transmitting neuronal signals and regulating a variety of biological events
Treg cells, which are developed in the thymus, peripherally differentiated Treg cells a Evidence to date suggests that nicotinic acetylcholine receptors (nAChRs) expression and function differ among T-cell recognized as induced Treg cells
We investigated the effect of nicotine on induced Treg (iTreg) cells, along with the expression patterns and mechanisms regulating nAChR
Summary
Cholinergic neurotransmitters and their corresponding nicotinic acetylcholine receptors (nAChRs) play pivotal roles in transmitting neuronal signals and regulating a variety of biological events. We have demonstrated that antigen-induced airway inflammation developed in immunized mice is largely dependent on CD4+ T cells [7]. In addition to Th subsets, regulatory T (Treg) cells play a pivotal role in immu regulation. Treg cells, which are developed in the thymus, peripherally differentiated Treg cells a Evidence to date suggests that nAChR expression and function differ among T-cell recognized as induced Treg (iTreg) cells. In addition to Th subsets, regulatory T (Treg) cells play a pivotal role in immune. The possible contribution of α7-nAChR to the development on iTreg cells, along with the expression patterns and mechanisms regulating nAChR of T-cell subsets was demonstrated [16], the participation pression, in comparison with other. We investigated the effect of nicotine on iTreg cells, along with the expression patterns and mechanisms regulating nAChR. 2.expression, Results in comparison with other T-cell subsets
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