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, the Karolinska Institutet Center for Innovative Medicine (Y.T.B.), the Swedish Childhood Cancer Foundation (J.-I.H., Y.T.B., M.M.), as well as the Stockholm County Council, the Swedish Cancer Foundation, and the Swedish Research Council (J.-I.H., Y.T.B.), the Cancer and Allergy Foundation of Sweden (J.-I.H.), the German Ministry of Education and Research (grant no. BMBF 01EO1303), and the German Research Foundation (grant no. SFB1160, TP1; S.E.). B.T. is also supported by a doctoral student scholarship from the Board of Postgraduate Studies at Karolinska Institutet. Computations were performed on resources provided by the Swedish National Infrastructure for Computing (SNIC) through the Uppsala Multidisciplinary Center for Advanced Computational Science under Project SNIC b2012204 and b2015280. Disclosure of potential conflict of interest: S. Ehl reports a grant from Deutsche Forschungsgemeinschaft (grant no. SFB1160 TP4) and a grant from BMBF (grant no. BMBF 01EO1303) during the conduct of the study and grants from Union Chimique Belge outside the submitted work. J.-I. Henter reports grants from the Swedish Childhood Cancer Foundation, the Swedish Cancer Foundation, the Swedish Research Council, the Stockholm County Council, and the Cancer and Allergy Foundation of Sweden during the conduct of the study. M. Meeths reports grants from the Swedish Childhood Cancer Foundation during the conduct of the study. The rest of the authors declare that they have no relevant conflicts of interest.

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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, antigenspecific 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.

This study has contributed to a better understanding of clinical features of AR in China.