(A) The proximity of cholinergic brain neurons to glia and the presence of AChRs on immune cells facilitate the cholinergic neuroimmune regulation. In peripheral tissues, communication of the ACh eliciting vagus nerve with the norepinephrine (NE) producing splenic nerve activates ACh production in T cells, where ACh initiates the cholinergic anti-inflammatory pathway by α7 nAChR activation and the suppression of pro-inflammatory cytokines secretion from splenic macrophages. (B) Molecular mechanisms involved in cholinergic anti-inflammatory actions involve the α7 nAChR-induced anti-inflammatory response that (1) inhibits the NF-κB pathway [43], (2) activates the JAK-STAT3 pathway (2) [41,45] or (3) up-regulates IRAK-M that attenuates TLR signaling (3) [46]. In addition, inflammatory stimuli up-regulate CHRNA7 and down-regulate its duplicated fused gene CHRFAM7A (4), thus promoting the anti-inflammatory actions [49].