Prof. Shen-Bin Liu
Somatosensory-autonomic reflexes for modulating immune homeostasis by acupuncture
Address: Room B4028, Institute of Brain Science, Fudan University, 131 Dongan Road, Shanghai, China, 200032
Dr. Shenbin Liu received his Ph.D. at the Fudan University in 2016. From 2016 to 2021, he obtained the post-doctoral training under Dr.Qiufu Ma in the department of neurobiology at the Harvard Medical School and the department of cancer biology at the Dana-Farber Cancer Institute. He joined the Institutes of Brain Science at Fudan University in 2021.
(1) The neuroanatomical mechanism for acupuncture to modulating immune homeostasis.
(2) The cross-talk between the autonomic nervous system and the immune system.
The interaction between the brain and the immune system plays a vital role for immune regulation, defense response and homeostasis. The brain via the autonomic nerve and neuroendocrine pathways to modulate peripheral immune cells’ function. Information about peripheral immune cells’ activity can be transmitted to the brain by humoral and neural pathways. Autonomic neurons and immune cells are highly diversity and heterogeneous. Our lab deploys multiple genetic strategy, takes a multidisciplinary approach using electrophysiological, physiological detection system, flow cytometry methods in combination of non-invasive bioelectric stimulation (eg. acupuncture) to identification of autonomic neurons/immune cells and molecules that are critically involved in the pathogenesis of autoimmune and infectious diseases. Our long-term goal is to provide novel insights into the nerve-immune connection in chronic diseases and development of effective therapeutic ways and drugs.
1. Liu S#, Wang Z#, Su Y, Qi L, Yang W, Fu M, Jing X, Wang Y, Ma Q*(2021). Identification of sensory neurons that somatotopically drive the vagal-adrenal anti-inflammatory axis. Nature. 598(7882):641-645
2. Liu S, Wang ZF, Su YS, Ray RS, Jing XH, Wang YQ, Ma Q*(2020). Somatotopic organization and intensity dependence in driving distinct NPY-expressing sympathetic pathways by electroacupuncture. Neuron. S0896-6273 (20) 30532-8
3. Li Q#, Liu S#, Li L, Ji X, Wang M, Zhou J*(2019). Spinal IL-36γ/IL-36R participates in the maintenance of chronic inflammatory pain through astroglial JNK pathway. Glia. 67(3):438-451
4. Liu S#, Feng J#, Luo J, Yang P, Brett T, Hu H*(2016). Eact, a small molecule activator of TMEM16A, activates TRPV1 and elicits pain- and itch-related behaviors.Br J Pharmacol. 173(7):1208-18
5. Liu S#, Mi WL#, Li Q, Zhang MT, Hu S, Han P, Mao-Ying QL, Wang YQ*(2015). Spinal IL-33/ST2 Signaling Contributes to Neuropathic Pain via Neuronal CaMKII-CREB and Astroglial JAK2-STAT3 Cascades in Mice. Anesthesiology. 123(5):1154-69.