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Allergy. 2020 Mar 21. doi: 10.1111/all.14288. [Epub ahead of print]

CD23 expression on switched memory B cells bridges T-B cell interaction in allergic rhinitis.

Author information

1
Department of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
2
The University of Queensland Diamantina Institute, Faculty of Medicine, The University of Queensland, Brisbane, Australia.
3
Department of Immunology and Infectious Disease, John Curtin School of Medical Research, Australian National University, Canberra, Australia.
4
Laboratory of Immunology for Environment and Health, Shandong Analysis and Test Center, Qilu University of Technology (Shandong Academy of Sciences), Jinan, P.R. China.
5
Department of Otolaryngology-Head and Neck Surgery, Wisco General Hospital, China Resources, Wuhan, P.R. China.
6
Department of Allergy, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.

Abstract

BACKGROUND:

The contribution of B-cell subsets and T-B cell interaction to the pathogenesis of allergic rhinitis (AR) and mechanisms of allergen immunotherapy (AIT) remain poorly understood. This study aimed to outline circulating B-cell signature, the underlying mechanism, and its association with clinical response to AIT in patients with AR.

METHODS:

IgD/CD27 and CD24/CD38 core gating systems were used to determine frequencies and phenotypes of B cells. Correlations between B cells, T cells, antigen-specific IgE, and disease severity in AR patients were investigated. Switched memory B cells were co-cultured with type 2 follicular helper T (Tfh2) cells and follicular regulatory T (Tfr) cells. Associations between B-cell subsets and clinical benefits of AIT were analyzed.

RESULTS:

Frequencies and absolute numbers of circulating memory B cells were increased in AR patients. CD23 expression on CD19+ CD20+ CD27+ IgD- switched memory B cells was significantly enhanced and positively correlated with antigen-specific IgE levels, symptom scores, and Tfh2/Tfr cell ratio in AR patients. Compared to those from healthy controls, Tfh2 cells from AR patients had a greater capacity to induce CD23 expression on switched memory B cells via IL-4, which was unable to be sufficiently suppressed by AR-associated Tfr cells with defective IL-10 expression. CD23 expression on switched memory B cells was downregulated after 12-month AIT, which positively associated with disease remission in AR patients.

CONCLUSION:

T-B cell interaction, bridged by CD23 expression particularly on switched memory B cells, may be involved in the disease pathogenesis and mechanism of AIT in patients with AR.

KEYWORDS:

allergen immunotherapy; allergic rhinitis; immunoglobulin E; interaction; switched memory B cell

PMID:
32198890
DOI:
10.1111/all.14288

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