Current Allergy and Asthma Reports

, Volume 13, Issue 6, pp 596–606

Molecular Basis for Downregulation of C5a-Mediated Inflammation by IgG1 Immune Complexes in Allergy and Asthma

Immune Deficiency and Dysregulation (DP Huston, Section Editor)

DOI: 10.1007/s11882-013-0387-3

Cite this article as:
Pandey, M.K. Curr Allergy Asthma Rep (2013) 13: 596. doi:10.1007/s11882-013-0387-3


Allergy and asthma are triggered primarily by the binding of allergen-specific immunoglobulin E (IgE)–allergen complexes to their receptors, recognition of the allergens by antigen-presenting cells, and allergen presentation to the T cells. These events lead to mucus secretions, runny nose, itchy eyes, sneezing, airway hyperresponsiveness, and nasal congestion. Complement 5a (C5a) has emerged as a central molecule that mediates these allergic reactions. Many allergens and allergen-specific IgG immune complexes (IgG-ICs) cause complement activation and C5a generation. C5a interaction with its receptor (C5aR) leads to the infiltration and activation of several immunologic cell types and the secretion of pathogenic inflammatory and proinflammatory mediators. However, IgG1-IC binding to the IgG inhibitory Fc gamma receptor (FcγRIIB) suppresses C5aR-mediated inflammatory signaling and, hence, may reduce the inflammatory immune responses through this FcγRIIB-mediated pathway. Reviews of the IgG1-IC interactions with C5a-mediated inflammatory immune responses suggest that IgG1-IC–C5a inhibitory therapy may reduce inflammation in allergic diseases.


Allergen Glycosylated IgG Cytokines Immunologic cells Fcγ receptor Complement-5a receptor Allergen immunotherapy Allergy Asthma Leukocytes 

Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  1. 1.Division of Human Genetics Cincinnati Children’s Hospital Medical CenterCincinnatiUSA
  2. 2.Department of PediatricsUniversity of Cincinnati College of MedicineCincinnatiUSA

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