期刊
CELL
卷 171, 期 1, 页码 217-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2017.08.006
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资金
- LEO Pharma
- WUSM Institute of Clinical and Translational Sciences (ICTS)
- NIH National Center for Advancing Translational Sciences (NCATS) Clinical and Translational Science Award (CTSA) [UL1TR000448]
- NCI [P30CA91842]
- ICTS CTSA grant from the National Center for Research Resources (NCRR) [UL1TR000448]
- NCRR Shared Instrumentation grant [1S10RR027552]
- NIDDK [P30DK052574, R01DK103901]
- NINDS [R01NS042595]
- NIAMS [R21AR068012, K08AR065577, R01AR070116]
- NIGMS [R01GM101218]
- American Skin Association
- Doris Duke Charitable Foundation
- NHLBI [T32HL007317]
- Howard Hughes Medical Institute (HHMI) Medical Fellows Program
Mammals have evolved neurophysiologic reflexes, such as coughing and scratching, to expel invading pathogens and noxious environmental stimuli. It is well established that these responses are also associated with chronic inflammatory diseases, including asthma and atopic dermatitis. However, the mechanisms by which inflammatory pathways promote sensations such as itch remain poorly understood. Here, we show that type 2 cytokines directly activate sensory neurons in both mice and humans. Further, we demonstrate that chronic itch is dependent on neuronal IL-4Ra and JAK1 signaling. We also observe that patients with recalcitrant chronic itch that failed other immunosuppressive therapies markedly improve when treated with JAK inhibitors. Thus, signaling mechanisms previously ascribed to the immune system may represent novel therapeutic targets within the nervous system. Collectively, this study reveals an evolutionarily conserved paradigm in which the sensory nervous system employs classical immune signaling pathways to influence mammalian behavior.
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