CHAPEL HILL, N.C. — Today, a study co-authored by Onyinye I. Iweala, MD, PhD, of the UNC Division of Rheumatology, Allergy, and Immunology and the UNC Food Allergy Initiative has been accepted for publication in the Journal of Allergy and Clinical Immunology. The study found that select alpha-gal-specific human immunoglobulin E (IgE) clones can promote both alpha-gal-dependent and antigen-independent allergic effector cell activation.
The study, titled “Alpha-gal-specific human IgE promotes both alpha-gal-induced and antigen-independent allergic effector cell activation,” evaluated whether alpha-gal-specific immunoglobulin E (IgE), independent of other blood proteins, is sufficient to activate allergic effector cells. Using CRISPR technology, researchers generated an alpha-gal–deficient RBL cell line expressing human IgE receptors. Cells passively sensitized with sera from patients with alpha-gal syndrome or with select alpha-gal-specific human IgE clones demonstrated both alpha-gal-dependent and antigen-independent activation, as assessed by CD63 expression and mediator release assays.
These findings are groundbreaking, as the prevalence of alpha-gal was found to have risen over 5,500% since 2020 in a recent report. Scott P. Commins, MD, PhD, a contributing author, also reported that 96,000–450,000 persons in the United States might have been affected by Alpha Gal Syndrome since 2010.
The research team included Yinghui Wang, MBBS, MS; Yugen Zhang, DVM, PhD; Scott P. Commins, MD, PhD; and colleagues from the UNC Division of Rheumatology, Allergy, and Immunology, the Thurston Arthritis Research Center, and collaborating institutions.