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Spaceflight impairs antigen-specific tolerance induction in vivo and increases inflammatory cytokines

机译:太空飞行会削弱体内对抗原的特异性耐受诱导并增加炎症细胞因子

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摘要

The health risks of a dysregulated immune response during spaceflight are important to understand as plans emerge for humans to embark on long-term space travel to Mars. In this first-of-its-kind study, we used adoptive transfer of T-cell receptor transgenic OT-II CD4 T cells to track an in vivo antigen-specific immune response that was induced during the course of spaceflight. Experimental mice destined for spaceflight and mice that remained on the ground received transferred OT-II cells and cognate peptide stimulation with ovalbumin (OVA) 323-339 plus the inflammatory adjuvant, monophosphoryl lipid A. Control mice in both flight and ground cohorts received monophosphoryl lipid A alone without additional OVA stimulation. Numbers of OT-II cells in flight mice treated with OVA were significantly increased by 2-fold compared with ground mice treated with OVA, suggesting that tolerance induction was impaired by spaceflight. Production of proinflammatory cytokines were significantly increased in flight compared with ground mice, including a 5-fold increase in IFN-γ and a 10-fold increase in IL-17. This study is the first to show that immune tolerance may be impaired in spaceflight, leading to excessive inflammatory responses.—Chang, T. T., Spurlock, S. M, Candelario, T. L. T., Grenon, S. M., Hughes-Fulford, M. Spaceflight impairs antigen-specific tolerance induction in vivo and increases inflammatory cytokines.
机译:随着人类开始着手长期前往火星的计划的出现,在飞行过程中免疫反应失调对健康的危害非常重要。在这项同类研究中,我们采用了T细胞受体转基因OT-II CD4 T细胞的过继转移来追踪在航天过程中诱导的体内抗原特异性免疫反应。预定用于太空飞行的实验小鼠和留在地面的小鼠接受了转移的OT-II细胞,并用卵清蛋白(OVA)323-339加上炎性佐剂单磷酸脂A刺激了同源肽刺激。在飞行和地面队列的对照小鼠均接受了单磷酸脂一个没有额外的OVA刺激的人。与OVA处理的地面小鼠相比,OVA处理的飞行小鼠中OT-II细胞的数量显着增加了2倍,这表明航天诱导了耐受诱导。与地面小鼠相比,促炎性细胞因子的产生在飞行中显着增加,包括IFN-γ增加5倍,IL-17增加10倍。这项研究首次表明,航天飞行可能会削弱免疫耐受,导致过度的炎症反应。—Chang,TT,Spurlock,S.M,Candelario,TLT,Grenon,SM,Hughes-Fulford,M.航天会损害抗原。体内特异性耐受诱导并增加炎性细胞因子。

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