Cultural advice

The Australian National University acknowledges, celebrates and pays our respects to the Ngunnawal and Ngambri people of the Canberra region and to all First Nations Australians on whose traditional lands we meet and work, and whose cultures are among the oldest continuing cultures in human history.

Aboriginal and Torres Strait Islander peoples are advised that ANU Library collections may include images, names, voices, and other representations of deceased persons.

Material in the collection may contain terms, language or views that reflect the period in which the item was created and may be considered inappropriate today.

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

Loading...
Thumbnail Image

Date

Authors

Yao, Yin
Wang, Nan
Chen, Cai-Ling
Pan, Li
Wang, Zhi-Chao
Yunis, Joseph
Chen, Zhian
Zhang, Yu
Hu, Si-Tao
Xu, Xiao-Yan

Journal Title

Journal ISSN

Volume Title

Publisher

Blackwell Publishing Ltd

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 with 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.

Description

Citation

Source

Allergy

Book Title

Entity type

Access Statement

License Rights

Restricted until

2099-12-31