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首页> 外文期刊>Allergy >Regulation of allergen-induced bone marrow eosinophilopoiesis: role of CD4+ and CD8+ T cells.
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Regulation of allergen-induced bone marrow eosinophilopoiesis: role of CD4+ and CD8+ T cells.

机译：过敏原诱导的骨髓嗜酸性粒细胞生成的调节：CD4 +和CD8 + T细胞的作用。

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BACKGROUND: The mechanisms of the distant stimulation of the bone marrow (BM) after airway allergen exposure remain largely obscure. T cells have been implicated in allergic airway inflammation but their role in allergen-induced BM eosinophilopoiesis is poorly understood. The aim of this study was to determine the role of CD4(+) and CD8(+) T cells in allergen-induced BM eosinophilopoiesis. METHODS: Ovalbumin (OVA)-sensitized wild type (WT), CD4 knockout (CD4-/-) and CD8 knockout (CD8-/-) mice were exposed intranasally to OVA or saline. Bromo-deoxyuridine (BrdU) was used to label newly produced cells. Bone marrow, blood and bronchoalveolar lavage (BAL) were sampled 24 h after the final exposure. Immunostaining for newly produced eosinophils (i.e. BrdU(+)/MBP(+)) and BM eosinophil progenitor [CD34(+)/CD45(+)/interleukin-5 (IL-5)Ralpha(+)] cells was performed. RESULTS: The number of newly produced BM eosinophils (BrdU(+)/MBP(+) cells) was significantly reduced in allergen exposed CD4-/- or CD8-/- mice compared with allergen exposed WT mice, which was followed by a subsequent decrease in newly produced blood and airway eosinophils. Furthermore, BM eosinophil progenitors were significantly reduced in allergen exposed CD4-/- and CD8-/- mice compared with WT mice. Finally, serum IL-5 and Bronchoalveolar lavage fluid eotaxin-2 levels were abolished in allergen exposed CD4-/- mice to levels seen in saline exposed WT mice. CONCLUSIONS: These data suggests that both CD4(+) and CD8(+) T cells have a regulatory role in allergen-induced BM eosinophilopoiesis, whereas CD4(+) T cells are obligatory for allergen-induced airway eosinophilia. The subsequent traffic of eosinophils to the airways is likely to be at least partly regulated by a CD4(+) T-cell-dependent local airway eotaxin-2 production.
机译：背景：气道过敏原暴露后远距离刺激骨髓的机制仍然不清楚。 T细胞与过敏性气道炎症有关，但人们对它们在过敏原诱导的BM嗜酸性粒细胞生成中的作用了解甚少。这项研究的目的是确定CD4（+）和CD8（+）T细胞在变应原诱导的BM嗜酸性粒细胞生成中的作用。方法：将卵清蛋白（OVA）致敏的野生型（WT），CD4基因敲除（CD4-/-）和CD8基因敲除（CD8-/-）小鼠经鼻内暴露于OVA或生理盐水中。溴脱氧尿苷（BrdU）用于标记新产生的细胞。最后一次暴露后24小时，采集骨髓，血液和支气管肺泡灌洗液（BAL）。对新产生的嗜酸性粒细胞（即BrdU（+）/ MBP（+））和BM嗜酸性粒细胞祖细胞[CD34（+）/ CD45（+）/ interleukin-5（IL-5）Ralpha（+）]进行免疫染色。结果：与暴露于变应原的WT小鼠相比，暴露于变应原的CD4-/-或CD8-/-小鼠中新产生的BM嗜酸性粒细胞（BrdU（+）/ MBP（+）细胞）的数量显着减少，随后是随后的新产生的血液和气道嗜酸性粒细胞减少。此外，与WT小鼠相比，在暴露于变应原的CD4-/-和CD8-/-小鼠中，BM嗜酸性粒细胞祖细胞显着减少。最后，将暴露于变应原的CD4-/-小鼠的血清IL-5和支气管肺泡灌洗液中的eotaxin-2水平消除，使其与暴露于盐水的WT小鼠相同。结论：这些数据表明，CD4（+）和CD8（+）T细胞在变应原诱导的BM嗜酸性粒细胞生成中起调节作用，而CD4（+）T细胞对于变应原诱导的气道嗜酸性粒细胞增生是必需的。嗜酸性粒细胞随后向气道的运输可能至少部分受CD4（+）T细胞依赖性局部气道嗜酸性粒细胞趋化因子2产生的调节。

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