抗原提示細胞上に発現するα7ニコチン性アセチルコリン受容体 (α7 nAChR) は、CD4<sup>+</sup> T細胞の分化を抑制する

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  • α7 Nicotinic acetylcholine (ACh) receptors (α7 nAChRs) expressed on antigen-presenting cells (APCs) suppress the differentiation of CD4<sup>+</sup> T cells.

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<p>All the immune cells such as T cells, macrophages and dendritic cells (DCs), have ACh-synthesizing ability and express α7 nAChRs involved in regulation of proliferation, and synthesis of antigen-specific antibodies and proinflammatory cytokines. We investigated role of α7 nAChRs on APCs in regulation of CD4+ T cell differentiation. Spleen cells, including naïve CD4+ T cells and APCs (macrophages and DCs), were isolated from ovalbumin (OVA)-specific TCR transgenic DO11.10 mice, and cultured with OVA in the presence of GTS-21, an α7 nAChR agonist. GTS-21 suppressed the OVA-activated CD4+ T cell differentiation into regulatory T cells (Tregs), Th1, Th2 and Th17 cells. GTS-21 inhibited the production of Th cytokines (IFN-γ, IL-4 and IL-17). GTS‑21 inhibited differentiation into Tregs of OVA-induced CD4+ T cells co-cultured with APCs from the wild-type (WT) mice but did not affect differentiation of T cells co-cultured with APCs from α7 nAChR-deficient mice. These results suggest a critical role of α7 nAChRs on APCs in regulation of CD4+ T cell differentiation, and that α7 nAChR agonists and antagonists could be potentially useful agents for immune response modulation and enhancement.</p>

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