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<p>Regulatory T (Treg) cells are effective immunomodulators of adaptive and innate immune responses. Our previous studies have demonstrated that B-cell-induced CD4<sup>+</sup>Foxp3<sup>−</sup> regulatory T cells, referred to as Treg-of-B cells, exert suppressive capacity, by inhibiting CD4<sup>+</sup>CD25<sup>−</sup> T-cell proliferation and inflammasome activation. In the present study, Treg-of-B cells downregulated proinflammatory M1-like markers and partially induced M2-associated genes in unpolarized bone marrow-derived macrophages (BMDMs), as evidenced by RNA expression of <i>Nos2</i>, <i>Arg1</i>,<i> Retnla</i>,<i> Mrc1</i>, and <i>Egr2</i>. Treg-of-B cells decreased the RNA levels of <i>Nos2</i>, <i>Tnfa</i>, <i>Cd86</i>, and <i>Cxcl9</i>, and reduced the production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and nitrite in LPS/interferon (IFN)-γ-stimulated M1-like macrophages in a dose-dependent manner. These cells also secreted Th2 cytokines, including IL-10, IL-4, and IL-13, with enhanced cytokine production observed when cocultured with macrophages. Mechanistically, Treg-of-B cells exerted their modulatory effects via both cell-cell contact and contact-dependent induction of soluble mediators, particularly Th2 cytokines. Furthermore, Treg-of-B cells promoted IκBα accumulation and suppressed RNA expression of Kruppel-like factor 4 (<i>Klf4</i>), thereby inhibiting NF-κB activation. These findings suggest that Treg-of-B cells regulate macrophage plasticity and might prevent excessive inflammation.</p>

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B cells induced regulatory T cells attenuated the classical M1 polarization of mouse bone marrow-derived macrophages

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月10日

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  • Yi-Ping Huang,
  • Chien-Hui Chien,
  • Li-Chieh Wang,
  • Bor-Luen Chiang

摘要

Regulatory T (Treg) cells are effective immunomodulators of adaptive and innate immune responses. Our previous studies have demonstrated that B-cell-induced CD4+Foxp3− regulatory T cells, referred to as Treg-of-B cells, exert suppressive capacity, by inhibiting CD4+CD25− T-cell proliferation and inflammasome activation. In the present study, Treg-of-B cells downregulated proinflammatory M1-like markers and partially induced M2-associated genes in unpolarized bone marrow-derived macrophages (BMDMs), as evidenced by RNA expression of Nos2, Arg1, Retnla, Mrc1, and Egr2. Treg-of-B cells decreased the RNA levels of Nos2, Tnfa, Cd86, and Cxcl9, and reduced the production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and nitrite in LPS/interferon (IFN)-γ-stimulated M1-like macrophages in a dose-dependent manner. These cells also secreted Th2 cytokines, including IL-10, IL-4, and IL-13, with enhanced cytokine production observed when cocultured with macrophages. Mechanistically, Treg-of-B cells exerted their modulatory effects via both cell-cell contact and contact-dependent induction of soluble mediators, particularly Th2 cytokines. Furthermore, Treg-of-B cells promoted IκBα accumulation and suppressed RNA expression of Kruppel-like factor 4 (Klf4), thereby inhibiting NF-κB activation. These findings suggest that Treg-of-B cells regulate macrophage plasticity and might prevent excessive inflammation.