Abstract

Mast cells (MCs) are located in the periphery as well as the central nervous system (CNS). Known for sterile inflammation, MCs play a critical role in neuroinflammation, which is facilitated by their close proximity to nerve fibers in the periphery and meninges of the spinal cord and the brain. Multifaceted activation of MCs releasing neuropeptides, cytokines and other mediators has direct effects on the neural system as well as neurovascular interactions. Emerging studies have identified the release of extracellular traps, a phenomenon traditionally meant to ensnare invading pathogens, as a cause of MC-induced neural injury. In this review article, we will discuss mechanisms of MC interaction with the nervous system through degranulation, de novo synthesis, extracellular vesicles (EVs), tunneling nanotubes, and extracellular traps with implications across a variety of pathological conditions.

Highlights

  • Mast cells (MCs) are proinflammatory cells that are the first responders of the immune system (Galli et al, 2005; Gupta and Harvima, 2018)

  • It is suggested that MCs contribute to pathology through interaction with the vasculature and the central nervous system (CNS)

  • substance P (SP) along with IL33 causes MCs to increase secretion and gene expression of IL-1β (Taracanova et al, 2018). These responses were mediated by SP and IL-33 receptors, Neurokinin 1 (NK1) and small conductance Ca2+-activated K+ (SK2), respectively on MCs

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Summary

Introduction

Mast cells (MCs) are proinflammatory cells that are the first responders of the immune system (Galli et al, 2005; Gupta and Harvima, 2018). It is suggested that MCs contribute to pathology through interaction with the vasculature and the central nervous system (CNS). MCs have a delayed response leading to the release of cytokines, neuropeptides, and chemokines by de novo synthesis.

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