Reconciling neuronally and nonneuronally derived acetylcholine in the regulation of immune function.

Koichiro Kawashima, Takeshi Fujii, Yasuhiro Moriwaki, Hidemi Misawa, Kazuhide Horiguchi

Department of Molecular Pharmacology, Kitasato University School of Pharmacy, Tokyo, Japan. koichiro-jk@piano.ocn.ne.jp

Annals of the New York Academy of Sciences 2012 Jul

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Immune cells, including lymphocytes, express muscarinic and nicotinic acetylcholine (ACh) receptors (mAChRs and nAChRs, respectively), and agonist stimulation of these AChRs causes functional and biochemical changes in the cells. The origin of the ACh that acts on immune cell AChRs has remained unclear until recently, however. In 1995, we identified choline acetyltransferase mRNA and protein in human T> cells, and found that immunological T cell activation potentiated lymphocytic cholinergic transmission by increasing ACh synthesis and AChR expression. We also found that M(1) /M(5) mAChR signaling upregulates IgG(1) and proinflammatory cytokine production, whereas α7 nAChR signaling has the opposite effect. These findings suggest that ACh synthesized by T cells acts as an autocrine and/or paracrine factor via AChRs on immune cells to modulate immune function. In addition, a recently discovered endogenous allosteric α7 nAChR ligand, SLURP-1, also appears to be involved in modulating normal T cell function. © 2012 New York Academy of Sciences.

Citation

Koichiro Kawashima, Takeshi Fujii, Yasuhiro Moriwaki, Hidemi Misawa, Kazuhide Horiguchi. Reconciling neuronally and nonneuronally derived acetylcholine in the regulation of immune function. Annals of the New York Academy of Sciences. 2012 Jul;1261:7-17