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首页> 外文期刊>The journal of immunology >Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice
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Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice

机译：靶向CD25和糖皮质激素诱导的TNF受体家族相关基因表达T细胞差异性调节哮喘和正常母鼠后代的哮喘风险

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Immunological mechanisms leading to increased asthma susceptibility in early life remain obscure. In this study, we examined the effects of neonatal Ab treatments targeting T cell populations on the development of an asthma syndrome. We used a model of increased asthma susceptibility where offspring of asthmatic BALB/c mother mice are more prone (than normal pups) to develop the disease. Neonatal pretreatment of naive pups with mAb directed against the IL-2Rα chain (CD25), the costimulatory molecule glucocorticoid-induced TNFR family related gene, and the inhibitory molecule CTLA-4 elicited contrasting effects in offspring depending on the mother’s asthma status. Specifically, neonatal CD25high T cell depletion stimulated asthma susceptibility in normal offspring whereas it ameliorated the condition of pups born of asthmatic mothers. Conversely, glucocorticoid-induced TNFR family related gene ligation as a primary signal reduced the spleen cellularity and largely abrogated asthma susceptibility in asthma-prone offspring, without inducing disease in normal pups. Striking changes in Th1/Th2 cytokine levels, especially IL-4, followed mAb pretreatment and were consistent with the impact on asthma susceptibility. These results point to major differences in neonatal T cell population and responsiveness related to maternal asthma history. Interventions that temporarily remove and/or inactivate specific T cell subsets may therefore prove useful to attenuate early life asthma susceptibility and prevent the development of Th2-driven allergic airway disease.
机译：导致早期生命中哮喘易感性增加的免疫机制仍然不清楚。在这项研究中，我们检查了针对T细胞群的新生儿Ab治疗对哮喘综合征发展的影响。我们使用了哮喘易感性增加的模型，其中哮喘BALB / c母鼠的后代更容易（比正常幼崽）患病。新生幼稚犬针对IL-2Rα链（CD25）的单抗，共刺激分子糖皮质激素诱导的TNFR家族相关基因以及抑制分子CTLA-4的新生儿预处理，在后代中会产生不同的影响，具体取决于母亲的哮喘状况。具体而言，新生儿CD25高T细胞耗竭可刺激正常后代的哮喘易感性，而改善了哮喘母亲所生幼崽的状况。相反，糖皮质激素诱导的TNFR家族相关基因的连接作为主要信号降低了易患哮喘的后代的脾细胞数量，并大大消除了哮喘的易感性，而没有引起正常幼犬的疾病。在mAb预处理后，Th1 / Th2细胞因子的水平发生了惊人的变化，尤其是IL-4，这与对哮喘易感性的影响一致。这些结果表明，新生儿T细胞数量和与母亲哮喘史有关的反应性存在重大差异。因此，暂时去除和/或灭活特定T细胞亚群的干预措施可能被证明有助于减轻早期哮喘的易感性并防止Th2驱动的过敏性气道疾病的发展。

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