Volume 24, No 11, Nov 2014
ISSN: 1001-0602
EISSN: 1748-7838 2018
impact factor 17.848*
(Clarivate Analytics, 2019)
Volume 24 Issue 11, November 2014: 1374-1377
LETTERS TO THE EDITOR
Nociceptive neurons regulate innate and adaptive immunity and neuropathic pain through MyD88 adapter
Xing-Jun Liu1,*, Yanli Zhang2,3,*, Tong Liu1,4,*, Zhen-Zhong Xu1, Chul-Kyu Park1, Temugin Berta1, Dianhua Jiang2 and Ru-Rong Ji1
1Departments of Anesthesiology and Neurobiology, Duke University Medical Center, Durham, NC 27710
2Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA
3State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Peking Union Medical College; Chinese Academy of Medical Sciences, Beijing 100005, China
4Current address: Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, Soochow University, Suzhou, Jiangsu 215006, China
Correspondence: Ru-Rong Ji, E-mail: ru-rong.ji@duke.edu; Dianhua Jiang,(Dianhua.jiang@cshs.org)
Neural-immune interaction in health and disease is a hot topic in current biomedical research1,2. While the central nervous system (CNS) regulates systemic immune responses through hormonal and neuronal route, the peripheral nervous system (PNS) appears to modulate local innate immune responses1. Our organs are heavily innervated by the peripheral nerves, yet, it is not fully understood how the PNS controls immunity2. Toll-like receptors (TLRs) are traditionally expressed in immune cells to regulate innate immunity, but recent studies indicated that TLRs (such as TLR3, 4 and 7) are also expressed in primary sensory neurons, especially nociceptive neurons in dorsal root ganglia (DRGs) and trigeminal ganglia of the PNS to regulate sensory functions such as pain and itch3,4,5,6. TLR signaling is largely mediated by the myeloid differentiation factor 88 (MyD88) protein (but see7), and activation of MyD88 in turn activates the NF-κB and MAP kinase pathways, leading to the production of inflammatory cytokines and chemokines for the initiation of innate immunity3. Increasing evidence suggests that nociceptor neurons play a critical role in host defense and inflammation8,9. However, the key signaling molecules in nociceptors for the regulation of immunity remain to be identified. To this end, we generated MyD88-conditional knockout (CKO) mice by deleting MyD88 in nociceptive neurons expressing the sodium channel subunit Nav1.88,9.
10.1038/cr.2014.106
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