Department of Medicine and Department of Microbiology, Asthma and Allergic Disease Center, University of Virginia Health System, Charlottesville, Virginia, USA.
Address correspondence to: Larry Borish, Asthma and Allergic Disease Center, Box 801355, Charlottesville, Virginia 22903, USA. Phone: 434.243.6570; Email: firstname.lastname@example.org.
First published September 21, 2020 - More info
Allergic disorders include food allergy, allergic rhinitis, and certain forms of asthma resulting from the inappropriate development of immune responses to otherwise innocuous aeroallergens and foods. In this issue of the JCI, Thouvenot and Roitel et al. explore transcription infidelity as a mechanism that underlies the ability of these benign proteins to become allergens. Some foods and bioaerosols that produce allergies have RNA polymerase with a propensity to generate RNA gaps, thereby causing translational frameshifts. These frameshifts often create cationic carboxy-terminus residues that replace hydrophobic amino acids and have enhanced MHC binding, resulting in the tendency to provoke immune responses. IgE antibody responses initiated by these variant transcripts can later lead to IgE against the native molecule and also explain how anaphylaxis may occur in individuals who lacked specific IgE when tested using native protein reagents. This study has the potential to transform the diagnosis and treatment of allergic disorders.
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