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首页> 外文期刊>Mucosal immunology >Regulatory B cells from hilar lymph nodes of tolerant mice in a murine model of allergic airway disease are CD5 ~+, express TGF-β, and co-localize with CD4 ~+ Foxp3 ~+ T cells
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Regulatory B cells from hilar lymph nodes of tolerant mice in a murine model of allergic airway disease are CD5 ~+, express TGF-β, and co-localize with CD4 ~+ Foxp3 ~+ T cells

机译:在变应性气道疾病的小鼠模型中,耐受小鼠肺门淋巴结的调节性B细胞为CD5〜+,表达TGF-β,并与CD4〜+ Foxp3〜+ T细胞共定位

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摘要

In a biphasic, ovalbumin (OVA)-induced murine asthma model where allergic airway disease is followed by resolution and the development of local inhalational tolerance (LIT), transforming growth factor (TGF)-β-expressing CD5 ~+ B cells were selectively expanded locally in hilar lymph nodes (HLN) of LIT mice. LIT HLN CD5 ~+ B cells, but not LIT HLN CD5 ~+-B cells, induced expression of Foxp3 ~+ in CD4 ~+ CD25-T cells in vitro. These CD5 ~+ regulatory B cells (Breg) and CD4 ~+ Foxp3 ~+ T cells demonstrated similar increases in expression of chemokine receptors (CXCR4 and CXCR5) and co-localized in HLN B cell zones of LIT mice. The adoptive transfer of LIT HLN CD5 ~+ B cells, but not LIT HLN CD5 ~+-B cells, increased the number of CD4 ~+ Foxp3 ~+ T cells in the lung and inhibited airway eosinophilia in this OVA model. Thus, Breg in HLNs of LIT mice reside in a CD5 ~+ TGF-β-producing subpopulation and co-localize with CD4 ~+ Foxp3 ~+ T cells.
机译:在卵白蛋白(OVA)诱导的双相小鼠哮喘模型中,过敏性气道疾病随后得到解决并发生了局部吸入耐受(LIT),选择性转化了表达转化生长因子(TGF)-β的CD5〜+ B细胞局部位于LIT小鼠的肺门淋巴结(HLN)中。 LIT HLN CD5〜+ B细胞而非LIT HLN CD5〜+ -B细胞在体外诱导CD4〜+ CD25-T细胞中Foxp3〜+的表达。这些CD5〜+调节性B细胞(Breg)和CD4〜+ Foxp3〜+ T细胞表现出趋化因子受体(CXCR4和CXCR5)的表达相似增加,并且共定位于LIT小鼠的HLN B细胞区域。在这种OVA模型中,LIT HLN CD5〜+ B细胞的过继转移而不是LIT HLN CD5〜+ -B细胞的过继转移增加了肺中CD4〜+ Foxp3〜+ T细胞的数量,并抑制了气道嗜酸性粒细胞增多。因此,LIT小鼠的HLN中的Breg驻留在产生CD5〜+TGF-β的亚群中,并与CD4〜+ Foxp3〜+ T细胞共定位。

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