ArticleFrontiers in immunology2026
Putative α7-selective ligands interact with α9-containing nicotinic acetylcholine receptors and modulate immune functions of human mononuclear phagocytes.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Nicotinic acetylcholine receptors (nAChRs) on immune cells are promising therapeutic targets for the treatment of inflammatory diseases and pain. Both α7 and α9* nAChRs (*denotes the potential presence of other nAChR subunits) have been implicated as mediators of the cholinergic anti-inflammatory system (CAS). This study investigated the binding sites of α7-selective ligands on these receptors and their effects on ATP-dependent release of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 by human mononuclear phagocytes. Materials and Methods: The effects of classical ligands (e.g. ACh, nicotine), unconventional (phosphocholine), putative α7-specific ligands (S24795, PNU-282987 and methyllycaconitine), on the ATP-induced IL-1β release were studied in lipopolysaccharide-primed human monocytic THP-1 cells and THP-1-derived macrophages. Electrophysiological two-electrode voltage-clamp measurements were conducted on Results: In cytokine-release experiments, the nAChR agonists efficiently inhibited ATP-mediated IL-1β release. This inhibitory effect was reversed by specific antagonistic conopeptides [V11L;V16D]ArIB (α7 antagonist) and RgIA4 (α9 and α9α10 antagonist), indicating the involvement of nAChRs containing subunits α7, α9 and/or α10. Electrophysiological measurements suggested an interaction of putative α7-specific ligands with human α9* nAChRs. In molecular docking simulations, all tested ligands showed reasonable binding affinity to homomeric α7, α9 and α10 nAChR models near the C-loop region of the binding pocket. Conclusion: Our findings provide a more nuanced framework for interpreting the roles of nAChR subtypes in non-neuronal immune modulation, highlighting the complexity and potential importance of α9* nAChRs in the context of inflammation and innate immunity. The results underscore the importance of considering the nAChR subunit α9 when developing α7-selective ligands for immunomodulation and provides novel insights into the role of α9* nAChRs as potential therapeutic targets for inflammatory diseases and pain.
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