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Fang wang, Anna M Trier, Fengxian Li, Seonyoung Kim, Zhen Chen, Jiani N Chai, Madison R Mack, Stephanie A Morrison, Jennifer D Hamilton, Jinok Baek, Ting-Lin B Yang, Aaron M Ver Heul, Amy Z Xu, Zili Xie, Xintong Dong, Masato Kubo, Hongzhen Hu, Chyi-Song Hsieh, Xinzhong Dong, Qin Liu, David J Margolis, Marius Ardeleanu, Mark J Miller, Brian S Kim, A Basophil-Neuronal Axis Promotes Itch Flares, The Journal of Immunology, Volume 206, Issue 1_Supplement, May 2021, Page 23.12, https://doi.org/10.4049/jimmunol.206.Supp.23.12
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Abstract
Itch is an evolutionarily conserved sensation that facilitates expulsion of pathogens and noxious stimuli from the skin. However, in organ failure, cancer, and chronic inflammatory disorders like atopic dermatitis (AD), itch becomes chronic, intractable, and debilitating. Recent discoveries have implicated type 2 cell-associated cytokines such as IL-4, IL-13, and IL-31 in directly stimulating sensory neurons to promote chronic itch in AD. However, in addition to chronic itch, patients often experience intense acute itch exacerbations. Whether this form of itch represents amplification of known itch pathways or a different mechanism remains overlooked. Herein, we show that a large proportion of patients with AD harbor allergen-specific IgE and exhibit a propensity for acute itch flares. In mice, we found that while acute itch is mediated by the classical mast cell-histamine axis in steady-state, AD-associated inflammation renders this pathway dispensable. Instead, a previously unrecognized basophil-leukotriene receptor (CysLTR2) axis emerges as critical for acute itch flares. By probing fundamental itch mechanisms, our study highlights a novel basophil-neuronal circuit that may underlie a variety of pathological neuroimmune processes.
