Detection of serum IgG autoantibodies to FcεRIα by ELISA in patients with chronic spontaneous urticaria

Abstract

Background Mast cells are a key effector cell in the pathogenesis of chronic spontaneous urticaria (CSU) and activated by circulating FcεRI-specific IgG as well as IgE. This study evaluated the prevalence of circulating autoantibodies to FcεRIα in the sera of CSU patients. Methods Eighty-eight patients with CSU and 76 healthy controls (HCs) were enrolled. To detect circulating autoantibodies (IgG/IgA/IgM) to FcεRIα, ELISA was done using YH35324 (as a solid phase antigen), and its binding specificity was confirmed by the ELISA inhibition test. The antibody levels were presented by the ratio of YH35324-preincubated to mock-preincubated absorbance values. Clinical and autoimmune parameters, including atopy, urticaria activity score (UAS), serum total/free IgE levels, serum antinuclear antibody (ANA) and autologous serum skin test (ASST) results, were assessed. The autoimmune group was defined if CSU patients had positive results to ASST and/or ANA. Results The ratio of serum IgG to FcεRIα was significantly lower in CSU patients than in HCs (P<0.05), while no differences were noted in serum levels of IgG to recombinant FcεRIα or IgA/IgM autoantibodies. The autoimmune CSU group had significantly lower ratios of IgG/IgA (not IgM) autoantibodies to FcεRIα than the nonautoimmune CSU group (P<0.05 for each). No significant associations were found between sex, age, atopy, urticaria duration, UAS, or serum total/free IgE levels according to the presence of IgG/IgA/IgM antibodies. Conclusions This study confirmed the presence of IgG to FcεRIα in the sera of CSU patients, especially those with the autoimmune phenotype.

Omalizumab for Patients with Chronic Spontaneous Urticaria: A Narrative Review of Current Status

“…However, the driving process of mast cell activation has been elucidated and reviewed recently by Dobrican et al [ 16 ], Hide and Kaplan [ 17 ], and Kaplan et al [ 18 ], and briefly summarized herein. In most patients with CSU, mast cell activation and degranulation are driven by autoimmunity—either immunoglobulin (Ig)E-mediated type I autoimmunity (or autoallergy) or type IIb autoimmunity by IgG autoantibodies to IgE and/or the IgE receptor FcεRI on mast cells [ 19 ] (and reviewed by Hennino et al [ 20 ] and Kolkhir et al [ 21 ] and considered in recent articles [ 22 , 23 ]). Mast cells may also be activated by other non-immunologic pathways including complement, stem cell factor, Toll-like receptors, Mas-related G protein-coupled receptor X2, and pathogen-associated and damage-associated molecular patterns; this aspect has been reviewed by Ansotegui et al [ 24 ].…”