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首页> 外文期刊>Nature >Immunosuppressive CD71~+ erythroid cells compromise neonatal host defence against infection
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Immunosuppressive CD71~+ erythroid cells compromise neonatal host defence against infection

机译：免疫抑制性CD71〜+红细胞破坏新生儿宿主抵抗感染的能力

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摘要

Newborn infants are highly susceptible to infection. This defect in host defence has generally been ascribed to the immaturity of neonatal immune cells; however, the degree of hyporesponsiveness is highly variable and depends on the stimulation conditions. These discordant responses illustrate the need for a more unified explanation for why immunity is compromised in neonates. Here we show that physiologically enriched CD71~+ erythroid cells in neonatal mice and human cord blood have distinctive immunosuppressive properties. The production of innate immune protective cytokines by adult cells is diminished after transfer to neonatal mice or after co-culture with neonatal splenocytes. Neonatal CD71~+ cells express the enzyme arginase-2, and arginase activity is essential for the immunosuppressive properties of these cells because molecular inhibition of this enzyme or supplementation with L-arginine overrides immunosup-pression. In addition, the ablation of CD71~+ cells in neonatal mice, or the decline in number of these cells as postnatal development progresses parallels the loss of suppression, and restored resistance to the perinatal pathogens Listeria monocytogenes and Escherichia coli. However, CD71~+ cell-mediated susceptibility to infection is counterbalanced by CD71~+ cell-mediated protection against aberrant immune cell activation in the intestine, where colonization with commensal microorganisms occurs swiftly after parturition. Conversely, circumventing such colonization by using antimicrobials or gnotobiotic germ-free mice overrides these protective benefits. Thus, CD71~+ cells quench the excessive inflammation induced by abrupt colonization with commensal microorganisms after parturition.
机译：新生婴儿极易感染。宿主防御系统的这种缺陷通常归因于新生儿免疫细胞的不成熟。然而，反应不足的程度是高度可变的，并取决于刺激条件。这些不一致的反应说明了需要对为什么免疫力在新生儿中受损的原因进行更统一的解释。在这里我们表明，新生小鼠和人脐带血中生理富集的CD71〜+红细胞具有独特的免疫抑制特性。成年细胞转移到新生小鼠后或与新生脾细胞共培养后，先天性免疫保护性细胞因子的产生减少。新生儿CD71〜+细胞表达精氨酸酶2酶，精氨酸酶活性对于这些细胞的免疫抑制特性必不可少，因为对该酶的分子抑制作用或补充L-精氨酸可克服免疫抑制作用。此外，新生小鼠中CD71〜+细胞的消融，或随着出生后的发展这些细胞数量的减少与抑制作用的丧失并恢复了对围生期病原体单核细胞增生李斯特菌和大肠杆菌的抵抗力有关。然而，CD71〜+细胞介导的对感染的敏感性被CD71〜+细胞介导的针对肠道中异常免疫细胞活化的保护所抵消，在肠道中分娩后迅速出现了共生微生物的定居。相反，通过使用抗微生物剂或gnotobiotic无菌小鼠来规避这种定植，将超越这些保护性优势。因此，CD71 +细胞在分娩后猝灭了由共生微生物突然定殖引起的过度炎症。

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  • 来源
    《Nature》 |2013年第7478期|158-162|共5页
  • 作者

    Shokrollah Elahi; James M. Ertelt; Jeremy M. Kinder; Tony T. Jiang; Xuzhe Zhang; Lijun Xin; Vandana Chaturvedi; Beverly S. Strong; Joseph E. Quails; Kris A. Steinbrecher; Theodosia A. Kalfa; Aimen F. Shaaban; Sing Sing Way;

  • 作者单位

    Division of Infectious Diseases and Perinatal Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

    Division of Infectious Diseases and Perinatal Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

    Division of Infectious Diseases and Perinatal Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

    Division of Infectious Diseases and Perinatal Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

    Division of Infectious Diseases and Perinatal Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

    Division of Infectious Diseases and Perinatal Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

    Division of Infectious Diseases and Perinatal Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

    Center for Fetal Cellular and Molecular Therapy,Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

    Division of Infectious Diseases and Perinatal Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

    Division of Gastroenterology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue,Cincinnati, Ohio 45229, USA;

    Division of Hematology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

    Center for Fetal Cellular and Molecular Therapy,Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

    Division of Infectious Diseases and Perinatal Institute, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229, USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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