# Der p1 Dendritic Cells Promote Regulatory B Cell Induced Immunotolerance Through IL-10/STAT3 in Allergic Rhinitis

## TL;DR

This study shows that Der p1 dendritic cells can help treat allergic rhinitis by boosting regulatory B cells through the IL-10/STAT3 pathway.

## Contribution

The study reveals a novel mechanism of immune tolerance in allergic rhinitis through Der p1 dendritic cells and regulatory B cells.

## Key findings

- Der p1-DCs induce Breg differentiation and suppress allergic symptoms in mice.
- IL-10 overexpression attenuates STAT3 phosphorylation in nasal mucosa.
- AIT restores peripheral Breg and Treg levels in AR patients.

## Abstract

Background/Objectives: Allergic rhinitis (AR) is a complex immune-mediated disorder characterized by defective regulatory mechanisms. Emerging evidence suggests that impaired immune tolerance mediated by regulatory B cell (Breg) plays a pivotal role in AR pathogenesis. This study investigates the therapeutic potential of Der p1 allergen-modified dendritic cells (DC) in enhancing Breg-mediated immunotherapy and explores novel mechanisms underlying AR immunomodulation. Methods: Breg and the inflammatory cytokines were detected before and after allergen immunotherapy (AIT) in AR patients. Dust mite gene-derived dendritic cells were used to induce Breg. AR mice were treated with Der p1-DCs, and changes in Breg and related inflammatory indicators, as well as the impact of the IL-10/STAT pathway on DC vaccine treatment, were observed. Results: Following 6-month AIT, AR patients exhibited significant alleviation of nasal symptoms alongside restored peripheral Breg and Treg. In vitro co-culture of Der p1-DC-induced Bregs with CD4+CD25−T cells revealed that IL-10 blockade markedly increased Th cell. In AR murine models, intraperitoneal Der p1-DC administration suppressed allergic symptoms, upregulated nasal mucosal IL-10 expression, and attenuated STAT3 phosphorylation via IL-10 overexpression. Conclusions: AIT establishes immune tolerance through Breg-mediated regulatory mechanisms, while Der p1-DCs potently induce Breg differentiation and drive tolerance induction via the IL-10/STAT3 signaling axis.