IgG in the control of FcεRI activation: a battle on multiple fronts

Front Immunol. 2024 Jan 11:14:1339171. doi: 10.3389/fimmu.2023.1339171. eCollection 2023.

Abstract

The rising global incidence of IgE-mediated allergic reactions poses a significant challenge to the quality of life of affected individuals and to healthcare systems, with current treatments being limited in effectiveness, safety, and disease-modifying capabilities. IgE acts by sensitizing the high-affinity IgE receptor FcεRI expressed by mast cells and basophils, tuning these cells for inflammatory degranulation in response to future allergen encounters. In recent years, IgG has emerged as an essential negative regulator of IgE-dependent allergic inflammation. Mechanistically, studies have proposed different pathways by which IgG can interfere with the activation of IgE-mediated inflammation. Here, we briefly summarize the major proposed mechanisms of action by which IgG controls the IgE-FcεRI inflammatory axis and how those mechanisms are currently applied as therapeutic interventions for IgE-mediated inflammation.

Keywords: FcγRIIB; IgE; allergy; antibody; basophils; degranulation; mast cells; sensitization.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Basophils / metabolism
  • Humans
  • Immunoglobulin E* / metabolism
  • Immunoglobulin G / metabolism
  • Inflammation / metabolism
  • Quality of Life*

Substances

  • Immunoglobulin E
  • Immunoglobulin G

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This project was supported by funding from the following grants: SNF grant 310030_179165 to MV; SNF grant 310030_185114 to MB; SNF grant P2BEP3_188262 to PE.