A Brain-Spleen Axis Regulates Humoral Immunity
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RESEARCH HIGHLIGHT
A Brain-Spleen Axis Regulates Humoral Immunity Bin Zhang1 • Jinjie Zhong2 • Zhihua Gao1
Received: 21 June 2020 / Accepted: 16 August 2020 Ó Shanghai Institutes for Biological Sciences, CAS 2020
A happy mood helps to build a flourishing immune system. Interactions between the nervous and immune systems have attracted the interest of researchers for decades. It is well known that external stressors can activate the hypothalamus to regulate immune responses via the hypothalamic-pituitary-adrenal cortex (HPA) axis [1]. As well, inflammatory stimuli can activate a rapid antiinflammatory reflex via the cholinergic vagus nerve pathway. An important target for the nervous systemelicited immune regulation is the spleen, a key organ where immune cells meet pathogens and antigens to trigger innate and adaptive immune responses. Notably, the spleen is mainly innervated by sympathetic nerves [2]. Genetic or surgical ablation of the splenic nerve attenuates endotoxintriggered innate immune responses and prevents the inhibition of tumor necrosis factor a provoked by vagus nerve stimulation under septic conditions [2–4], demonstrating the pivotal importance of the splenic nerve in antiinflammatory innate immunity. However, whether a direct neural pathway from the brain to the spleen regulates adaptive immunity remains unknown. Writing in Nature, Zhang and colleagues uncovered that appropriate stressactivated corticotropin-releasing hormone (CRH) neurons in the hypothalamic paraventricular nucleus and/or central nucleus of the amygdala (PVN/CeA) drive a neural & Zhihua Gao [email protected] 1
Neuroscience Research Center and Department of Neurology, The Second Affiliated Hospital, Key Laboratory of Medical Neurobiology of Zhejiang Province, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou 310058, China
2
School of Basic Medical Sciences, Zhejiang University, Hangzhou 310058, China
pathway to the spleen to regulate humoral immune defense (Fig. 1). To determine whether the splenic nerve is directly engaged in adaptive immune responses, Zhang et al. [5] surgically removed the nerve and reported that the antigeninduced formation of T cell-dependent splenic plasma cells (SPPCs) is reduced. By contrast, the formation of T cellindependent SPPCs is not affected upon splenic denervation, suggesting that the splenic nerve is necessary for antigen-triggered T cell-dependent adaptive immunity. Zhang et al. [5] further reported that direct exposure of B cells to acetylcholine (ACh) rather than norepinephrine affects SPPCs formation. Splenic nerves only release norepinephrine [2]. How is the noradrenergic signal shifted to a cholinergic signal in the spleen? A previous study revealed that a subset of CD4? and choline acetyltransferase (ChAT)-expressing T cells abutting the noradrenergic nerve endings in the spleen is able to produce ACh upon nerve stimulation. By releasing ACh, they relay the neural noradrenergic signal to ACh-responsive macrophages to
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