House dust mites activate nociceptor–mast cell clusters to drive type 2 skin inflammation

Serhan, Nadine; Basso, Lilian; Sibilano, Riccardo; Petitfils, Camille; Meixiong, James; Bonnart, Chrystelle; Reber, Laurent L.; Marichal, Thomas; Starkl, Philipp; Cenac, Nicolas; Dong, Xinzhong; Tsai, Mindy; Galli, Stephen J.; Gaudenzio, Nicolas

doi:10.1038/s41590-019-0493-z

Cited by 247 publications

(253 citation statements)

References 52 publications

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“…In contrast to another report, we found that Alternaria extract, which has serine protease activity, was also capable of inducing DRG release of Substance P and inhibition of CGRP ( Fig. S1) (Cayrol et al, 2018;Serhan et al, 2019). These data indicate that the capacity for sensory neuron activation and Substance P release may be shared amongst disparate allergens.…”

Section: Substance P Release From Sensory Neurons Induces Cd301b + DCcontrasting

confidence: 99%

“…Using potassium chloride (KCl) responsiveness as a marker of live neurons, we found that approximately 16% neurons were responsive to 5 papain ( Fig. 2C), a similar value to that reported for house dust mite responsive neurons (Serhan et al, 2019). TRPV1 expression defines a subset of nociceptive neurons that not only sense noxious heat, but also promote pruriceptive responses.…”

Section: Allergens Directly Activate a Population Of Sensory Neurons supporting

confidence: 76%

“…1A & B). Mast cells have been shown to play a role in amplifying sensory neuron activation and tissue inflammation by house dust mite (Serhan et al, 2019). To investigate whether mast cells were similarly involved in 10 the immediate sensory response to papain, we injected papain i.d.…”

Section: Allergens Induce Immediate and Transient Itch Responses In Nmentioning

confidence: 99%

“…Our data suggested that TRPV1 + sensory neurons directly sense cysteine protease 10 allergens and relay signals to promote the egress of local Th2-skewing CD301b + DCs to the dLN. Activated peptidergic TRPV1 + neurons can release Substance P in response to allergen exposure and CGRP in response to bacterial and fungal exposures (Baral et al, 2018;Chiu et al, 2013;Kashem et al, 2015;Pinho-Ribeiro et al, 2018;Serhan et al, 2019). CGRP release was shown to promote IL-23 secretion by CD301b + DCs after 15 infection with the fungus Candida (Cohen et al, 2019;Kashem et al, 2015).…”

Section: Substance P Release From Sensory Neurons Induces Cd301b + DCmentioning

confidence: 99%

“…One potential allergen sensor is the sensory nervous system, which is highly 20 concentrated in barrier epithelia, broadly responsive to many different stimuli, and directly activated in vitro by diverse enzymatically active allergens such as bee venom, house dust mites, and papain (Chen and Lariviere, 2010;Reddy and Lerner, 2010;Serhan et al, 2019;Talbot et al, 2016;Trier et al, 2019;Veiga-Fernandes and Mucida, 2016). Sensory neurons have been shown to be closely associated with Langerhans cells in the human epidermis and activation of corneal sensory neurons can lead to DC activation in the contralateral eye (Guzman et al, 2018;Hosoi et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

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Allergen-induced dendritic cell migration is controlled through Substance P release by sensory neurons

Aderhold

Dewan

Perner

et al. 2020

Preprint

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Dendritic cells (DCs) of the cDC2 lineage are necessary for the initiation of the allergic immune response and in the dermis are marked by their expression of CD301b.CD301b + dermal DCs respond to allergens encountered in vivo, but not in vitro. This suggests that another cell in the dermis may sense allergens and relay that information 5 to activate and induce the migration of CD301b + DCs to the draining lymph node. Using a model of cutaneous allergen exposure, we show that allergens directly activate TRPV1 + sensory neurons leading to itch and pain behaviors. Allergen-activated sensory neurons release the neuropeptide Substance P, which stimulates proximally located CD301b + DCs through MRGPRA1. Substance P induces CD301b + DC migration to the 10 draining lymph node where they initiate Th2 differentiation. Thus, sensory neurons act as primary sensors of allergens, linking exposure to activation of allergic-skewing DCs and the initiation of the allergic immune response. 15

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Section: Substance P Release From Sensory Neurons Induces Cd301b + DCcontrasting

confidence: 99%

Section: Allergens Directly Activate a Population Of Sensory Neurons supporting

confidence: 76%

Section: Allergens Induce Immediate and Transient Itch Responses In Nmentioning

confidence: 99%

Section: Substance P Release From Sensory Neurons Induces Cd301b + DCmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Allergen-induced dendritic cell migration is controlled through Substance P release by sensory neurons

Aderhold

Dewan

Perner

et al. 2020

Preprint

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A Phosphatase‐Mimetic Nano‐Stabilizer of Mast Cells for Long‐Term Prevention of Allergic Disease

et al. 2021

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Allergic diseases are pathological immune responses with significant morbidity, which are closely associated with allergic mediators as released by allergen-stimulated mast cells (MCs). Prophylactic stabilization of MCs is regarded as a practical approach to prevent allergic diseases. However, most of the existing small molecular MC stabilizers exhibit a narrow therapeutic time window, failing to provide long-term prevention of allergic diseases. Herein, ceria nanoparticle (CeNP-) based phosphatase-mimetic nano-stabilizers (PMNSs) with a long-term therapeutic time window are developed for allergic disease prevention. By virtue of the regenerable catalytic hotspots of oxygen vacancies on the surface of CeNPs, PMNSs exhibit sustainable phosphatase-mimetic activity to dephosphorylate phosphoproteins in allergen-stimulated MCs. Consequently, PMNSs constantly modulate intracellular phospho-signaling cascades of MCs to inhibit the degranulation of allergic mediators, which prevents the initiation of allergic mediator-associated pathological responses, eventually providing protection against allergic diseases with a long-term therapeutic time window.The prevalence of allergic diseases has increased dramatically to epidemic proportions worldwide. More than 25% of the people worldwide suffer from numerous allergic diseases, [1] including

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Neuroimmune interactions in peripheral tissues

Klose

Veiga-Fernandes

2021

Eur J Immunol

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Neuroimmune interactions have been revealed to be at the centre stage of tissue defence, organ homeostasis, and organismal physiology. Neuronal and immune cell subsets have been shown to colocalize in discrete tissue environments, forming neuroimmune cell units that constitute the basis for bidirectional interactions. These multitissue units drive coordinated neuroimmune responses to local and systemic signals, which represents an important challenge to our current views of mucosal physiology and immune regulation. In this review, we focus on the impact of reciprocal neuroimmune interactions, focusing on the anatomy of neuronal innervation and on the neuronal regulation of immune cells in peripheral tissues. Finally, we shed light on recent studies that explore how neuroimmune interactions maximise sensing and integration of environmental aggressions, modulating immune function in health and disease.

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House dust mites activate nociceptor–mast cell clusters to drive type 2 skin inflammation

Cited by 247 publications

References 52 publications

Allergen-induced dendritic cell migration is controlled through Substance P release by sensory neurons

Allergen-induced dendritic cell migration is controlled through Substance P release by sensory neurons

A Phosphatase‐Mimetic Nano‐Stabilizer of Mast Cells for Long‐Term Prevention of Allergic Disease

Neuroimmune interactions in peripheral tissues

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