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. Author manuscript; available in PMC: 2019 Feb 7.
Published in final edited form as: Bioelectron Med (Lond). 2018 May;1(2):151–165. doi: 10.2217/bem-2018-0001

Figure 1. Description of neuroimmune circuits with potential therapeutic use in the treatment of arthritis.

Figure 1.

An efferent vagus nerve can inhibit inflammation through the activation of splenic nerve (A) by a neuroimmune pathway constituted by alpha-7 nicotinic acetylcholine receptor (α7nAChR)-expressing mesenteric ganglia (B) and splenic acetylcholine-producing T lymphocytes. Afferent vagal signaling, sympathetic C1 neurons (G) and cortical stimulation (H) can prevent local joint inflammation by a mechanism dependent on activation of LC (F) followed by stimulation of splanchnic nerve (E) or synovial sympathetic innervations (C & D). An articular non-neural cholinergic system improves local inflammation by a mechanism dependent on a7nAchR expressed in macrophage/fibroblast (C) while a neural adrenergic system inhibits local inflammation by direct (β-adrenoceptors) or indirect (IL-10-producing B lymphocytes) mechanisms (D). A recent hypothesis suggests that non-neural acetylcholine can be produced by peripheral T-cells that migrate to organs (e.g., spleen) after vagal stimulation (I). LC: Locus coeruleus.