Revisiting the role of MRGPRX2 on hypersensitivity reactions to neuromuscular blocking drugs

Curr Opin Immunol. 2021 Oct:72:65-71. doi: 10.1016/j.coi.2021.03.011. Epub 2021 Apr 12.

Abstract

Anaphylaxis is caused by a variety of triggers including Food and Drug Administration (FDA)-approved antibiotics, contrast media and neuromuscular blocking drugs (NMBDs). Traditionally, drug-induced anaphylaxis was thought to result mainly from IgE-mediated histamine release from mast cells. Recently, a G protein-coupled receptor known as MRGPRX2 has been identified and shown to be highly expressed on human skin but not lung mast cells. The demonstration that many NMBDs induce degranulation in human mast cells via MRGPRX2 led to the idea that this receptor contributes to NMBD-induced hypersensitivity reactions. However, other studies have raised doubts regarding its role in drug-induced hypersensitivity. This review discusses the current status and controversy on MRGPRX2's role on NMBD-induced hypersensitivity.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Anaphylaxis / etiology
  • Anaphylaxis / metabolism
  • Animals
  • Biomarkers
  • Calcium / metabolism
  • Cell Degranulation / immunology
  • Disease Susceptibility*
  • Drug Hypersensitivity / etiology*
  • Drug Hypersensitivity / metabolism
  • Genetic Predisposition to Disease
  • Humans
  • Immunoglobulin E / immunology
  • Mast Cells / immunology
  • Mast Cells / metabolism
  • Mutation
  • Nerve Tissue Proteins / genetics*
  • Neuromuscular Blocking Agents / adverse effects*
  • Receptors, G-Protein-Coupled / genetics*
  • Receptors, IgE / metabolism
  • Receptors, Neuropeptide / genetics*

Substances

  • Biomarkers
  • MRGPRX2 protein, human
  • Nerve Tissue Proteins
  • Neuromuscular Blocking Agents
  • Receptors, G-Protein-Coupled
  • Receptors, IgE
  • Receptors, Neuropeptide
  • Immunoglobulin E
  • Calcium