Brain control of humoral immune responses amenable to behavioural modulation

Xu Zhang, Bo Lei, Yuan Yuan, Li Zhang, Lu Hu, Sen Jin, Bilin Kang, Xuebin Liao, Wenzhi Sun, Fuqiang Xu, Yi Zhong (), Ji Hu () and Hai Qi ()
Additional contact information
Xu Zhang: Tsinghua University
Bo Lei: Tsinghua University
Yuan Yuan: ShanghaiTech University
Li Zhang: Tsinghua University
Lu Hu: Tsinghua University
Sen Jin: Chinese Academy of Sciences
Bilin Kang: Tsinghua University
Xuebin Liao: Tsinghua University
Wenzhi Sun: Capital Medical University
Fuqiang Xu: Chinese Academy of Sciences
Yi Zhong: Tsinghua University
Ji Hu: ShanghaiTech University
Hai Qi: Tsinghua University

Nature, 2020, vol. 581, issue 7807, 204-208

Abstract: Abstract It has been speculated that brain activities might directly control adaptive immune responses in lymphoid organs, although there is little evidence for this. Here we show that splenic denervation in mice specifically compromises the formation of plasma cells during a T cell-dependent but not T cell-independent immune response. Splenic nerve activity enhances plasma cell production in a manner that requires B-cell responsiveness to acetylcholine mediated by the α9 nicotinic receptor, and T cells that express choline acetyl transferase1,2 probably act as a relay between the noradrenergic nerve and acetylcholine-responding B cells. We show that neurons in the central nucleus of the amygdala (CeA) and the paraventricular nucleus (PVN) that express corticotropin-releasing hormone (CRH) are connected to the splenic nerve; ablation or pharmacogenetic inhibition of these neurons reduces plasma cell formation, whereas pharmacogenetic activation of these neurons increases plasma cell abundance after immunization. In a newly developed behaviour regimen, mice are made to stand on an elevated platform, leading to activation of CeA and PVN CRH neurons and increased plasma cell formation. In immunized mice, the elevated platform regimen induces an increase in antigen-specific IgG antibodies in a manner that depends on CRH neurons in the CeA and PVN, an intact splenic nerve, and B cell expression of the α9 acetylcholine receptor. By identifying a specific brain–spleen neural connection that autonomically enhances humoral responses and demonstrating immune stimulation by a bodily behaviour, our study reveals brain control of adaptive immunity and suggests the possibility to enhance immunocompetency by behavioural intervention.

Date: 2020
References: Add references at CitEc
Citations: View citations in EconPapers (4)

Downloads: (external link)
https://www.nature.com/articles/s41586-020-2235-7 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:581:y:2020:i:7807:d:10.1038_s41586-020-2235-7

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/s41586-020-2235-7

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().