Neuroinflammation Modulation via α7 Nicotinic Acetylcholine Receptor and Its Chaperone, RIC-3

• Published in: Molecules (Basel, Switzerland) Vol. 26; no. 20; p. 6139
• Main Authors: Mizrachi, Tehila, Vaknin-Dembinsky, Adi, Brenner, Talma, Treinin, Millet
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 11.10.2021; MDPI
• Subjects: Acetylcholine receptors (nicotinic); Alzheimer's disease; Animal models; Antigens; Cell activation; Cell differentiation; Cell proliferation; Central nervous system; cholinergic anti-inflammatory pathway; Cholinergics; Cytokines; Dendritic cells; Deregulation; Differentiation; Experimental allergic encephalomyelitis; experimental autoimmune encephalomyelitis; Gene expression; Immune system; Inflammation; Kinases; Ligands; Multiple sclerosis; Musculoskeletal system; Nervous system; neuroinflammation; Neuromodulation; Nicotine; Parkinson's disease; Phosphorylation; Review; RIC-3; Roles; Schizophrenia; Sepsis; Smoking; α7 nicotinic acetylcholine receptor
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules26206139

Nicotinic acetylcholine receptors (nAChRs) are widely expressed in or on various cell types and have diverse functions. In immune cells nAChRs regulate proliferation, differentiation and cytokine release. Specifically, activation of the α7 nAChR reduces inflammation as part of the cholinergic anti-inflammatory pathway. Here we review numerous effects of α7 nAChR activation on immune cell function and differentiation. Further, we also describe evidence implicating this receptor and its chaperone RIC-3 in diseases of the central nervous system and in neuroinflammation, focusing on multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Deregulated neuroinflammation due to dysfunction of α7 nAChR provides one explanation for involvement of this receptor and of RIC-3 in neurodegenerative diseases. In this review, we also provide evidence implicating α7 nAChRs and RIC-3 in neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) involving neuroinflammation. Besides, we will describe the therapeutic implications of activating the cholinergic anti-inflammatory pathway for diseases involving neuroinflammation.