CD23+IgG1+ memory B cells are poised to switch to pathogenic IgE production in food allergy

Miyo Ota, Kenneth B. Hoehn, Weslley Fernandes-Braga, Takayuki Ota, Carlos J. Aranda, Sara Friedman, Mariana G.C. Miranda-Waldetario, Jamie Redes, Maria Suprun, Galina Grishina, Hugh A. Sampson, Alefiyah Malbari, Steven H. Kleinstein, Scott H. Sicherer, Maria A. Curotto de Lafaille

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


Food allergy is caused by allergen-specific immunoglobulin E (IgE) antibodies, but little is known about the B cell memory of persistent IgE responses. Here, we describe, in human pediatric peanut allergy, a population of CD23+IgG1+ memory B cells arising in type 2 immune responses that contain high-affinity peanut-specific clones and generate IgE-producing cells upon activation. The frequency of CD23+IgG1+ memory B cells correlated with circulating concentrations of IgE in children with peanut allergy. A corresponding population of “type 2-marked” IgG1+ memory B cells was identified in single-cell RNA sequencing experiments. These cells differentially expressed interleukin-4 (IL-4)- and IL-13-regulated genes, such as FCER2/CD23+, IL4R, and germline IGHE, and carried highly mutated B cell receptors (BCRs). In children with high concentrations of serum peanut-specific IgE, high-affinity B cells that bind the main peanut allergen Ara h 2 mapped to the population of “type 2-marked” IgG1+ memory B cells and included clones with convergent BCRs across different individuals. Our findings indicate that CD23+IgG1+ memory B cells transcribing germline IGHE are a unique memory population containing precursors of high-affinity pathogenic IgE-producing cells that are likely to be involved in the long-term persistence of peanut allergy.

Original languageEnglish
Article numbereadi0673
JournalScience Translational Medicine
Issue number733
StatePublished - 2024


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