M2 macrophages promote IL-10⁺B-cell production and alleviate asthma in mice.

IF 4.1 Q2 IMMUNOLOGY

Immunotherapy advances Pub Date : 2025-03-10 eCollection Date: 2025-01-01 DOI:10.1093/immadv/ltaf007

Baichao Yu, Xueqi Wang, Yongkun Zheng, Wenjun Wang, Xiaoqin Cheng, Yue Cao, Mingxing Wei, Ying Fu, Yiwei Chu, Luman Wang

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Abstract

Introduction: B cells have a central regulatory role in various diseases. While macrophages are found in the disease microenvironment and interact with tissue and diverse immune cells, their relationship with B cells remains poorly explored.

Methods: This study used an asthma animal model and macrophage depletion and demonstrated a significant exacerbation of asthma symptoms upon macrophage removal, coupled with a marked reduction in IL-10⁺ B-cell expression.

Results: Further analysis revealed that the macrophages interacting with IL-10⁺ B cells in the asthma microenvironment were of the M2 subtype. Furthermore, our sequencing data indicated a potential mechanism wherein M2 macrophages promote IL-10⁺ B-cell activity through the TGF-β pathway and oxidative phosphorylation pathways.

Conclusion: These findings suggest that M2 macrophages modulate IL-10⁺ B cells, ultimately mitigating asthma symptoms in mouse models.

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M2巨噬细胞促进IL-10+ b细胞生成，减轻小鼠哮喘。

B细胞在多种疾病中起着重要的调节作用。虽然巨噬细胞存在于疾病微环境中，并与组织和多种免疫细胞相互作用，但它们与B细胞的关系尚不清楚。方法：本研究采用哮喘动物模型和巨噬细胞去除，发现巨噬细胞去除后哮喘症状显著加重，同时IL-10+ b细胞表达显著降低。结果：进一步分析发现哮喘微环境中与IL-10+ B细胞相互作用的巨噬细胞为M2亚型。此外，我们的测序数据表明，M2巨噬细胞通过TGF-β途径和氧化磷酸化途径促进IL-10+ b细胞活性的潜在机制。结论：这些发现提示M2巨噬细胞调节IL-10+ B细胞，最终减轻小鼠哮喘症状。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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