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Related Experiment Video

Updated: Oct 5, 2025

Author Spotlight: Advancing Allergic Rhinitis Research with Multicolor Immunofluorescence

Author Spotlight: Advancing Allergic Rhinitis Research with Multicolor Immunofluorescence

Published on: September 22, 2023

CD38⁺ B cells affect immunotherapy for allergic rhinitis.

Gui-Xiang Tian¹, Ke-Ping Peng², Ming-Hui Liu¹

¹Department of Ultrasound, The Second Xiangya Hospital of Central South University, Changsha, China; Research Center of Ultrasonography, The Second Xiangya Hospital of Central South University, Changsha, China.

The Journal of Allergy and Clinical Immunology

|January 30, 2022

Summary

Antigen-specific CD38+ B cells hinder allergen-specific immunotherapy (AIT) by producing IL-6, which converts regulatory T cells. Inhibiting these B cells enhances AIT effectiveness in allergic rhinitis treatment.

Keywords:

Allergy B cell CD38 immunotherapy regulatory T cell

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Published on: September 20, 2019

Area of Science:

Immunology
Allergy Research
Cell Biology

Background:

Allergen-specific immunotherapy (AIT) is a primary treatment for allergic diseases, but its efficacy requires enhancement.
CD38-expressing B cells (CD38+ B cells) are implicated in allergic disease development and immune regulation.

Purpose of the Study:

To investigate the specific role of antigen-specific CD38+ B cells within the context of AIT.
To understand the mechanisms by which CD38+ B cells influence AIT outcomes.

Main Methods:

Analysis of AIT outcomes in 48 perennial allergic rhinitis (AR) patients using flow cytometry and ELISA.
Development of an AR murine model to assess the function of CD38+ B cells during AIT.
Assessment of peripheral blood immune cell populations and serum cytokine levels.

Main Results:

Antigen-specific CD38+ B cells were identified in AR patients and their frequency negatively correlated with AIT success.
A negative correlation was observed between CD38+ B cell frequency and regulatory T cell (Treg) frequency in patients undergoing AIT.
CD38+ B cells produced IL-6 upon antigen exposure, promoting the conversion of Tregs to T helper 17 (TH17) cells.
Administration of anti-CD38 antibody significantly improved AIT therapeutic effects.

Conclusions:

Antigen-specific CD38+ B cells impair AIT efficacy by driving Treg to TH17 cell differentiation via IL-6 production.
Targeting and inhibiting CD38+ B cells can significantly enhance the therapeutic benefits of AIT for allergic conditions.