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首页> 外文期刊>Infection and immunity >Preexisting Inflammation Due to Mycobacterium bovis BCG Infection Differentially Modulates T-Cell Priming against a Replicating or Nonreplicating Immunogen
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Preexisting Inflammation Due to Mycobacterium bovis BCG Infection Differentially Modulates T-Cell Priming against a Replicating or Nonreplicating Immunogen

机译：牛分枝杆菌BCG感染导致的既有炎症差异性调节了针对复制或非复制免疫原的T细胞启动

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Induction of T-cell memory by vaccination ensures long-term protection against pathogens. We determined whether on-going inflammatory responses during vaccination influenced T-cell priming. A preexposure of mice to Mycobacterium bovis BCG impaired their subsequent ability to prime T cells against Listeria monocytogenes. This was characterized by a decrease in L. monocytogenes-specific gamma interferon (IFN-γ)-secreting CD4+ and CD8+ T cells. The intensity of T-cell priming towards L. monocytogenes depended on the extent of L. monocytogenes expansion, and a cessation of this expansion caused by M. bovis BCG-induced inflammation resulted in impairment in T-cell priming. A challenge of M. bovis BCG-infected mice with a higher L. monocytogenes dose increased L. monocytogenes survival and restored T-cell priming towards L. monocytogenes. Impairment in T-cell priming towards L. monocytogenes due to M. bovis BCG-induced inflammation resulted in a compromised protective efficacy in the long term after mice were rechallenged with L. monocytogenes. Preexisting inflammation selectively impaired T-cell priming for replicating immunogens as CD8+ T-cell response to ovalbumin administered as an inert antigen (ovalbumin-archaeosomes) was enhanced by M. bovis BCG preimmunization, whereas priming towards ovalbumin administered as a live immunogen (L. monocytogenes-ovalbumin) was impaired. Thus, depending on the nature of the immunogen, the presence of prior inflammatory responses may either impede or boost vaccine efficacy.
机译：通过疫苗接种诱导T细胞记忆可确保长期防御病原体。我们确定了疫苗接种过程中持续的炎症反应是否影响了T细胞启动。小鼠预先暴露于牛分枝杆菌BCG会削弱它们随后针对T细胞抵抗单核细胞增生李斯特菌的能力。其特征在于 L的降低。单核细胞增生特异性γ干扰素分泌的CD4 + 和CD8 + T细胞。 T细胞向 L启动的强度。单核细胞增生病取决于 L的程度。单核细胞增生扩展，以及由 M引起的这种扩展的停止。牛BCG引起的炎症导致T细胞启动作用受损。 M的挑战。牛 BCG感染的小鼠具有更高的 L。单核细胞增生病剂量增加 L。单核细胞增生的存活和恢复的T细胞对 L的启动。单核细胞增生。 T细胞向 L启动的损害。单核细胞增生是由于 M。牛 L攻击后，长期牛牛BCG引起的炎症会导致保护功效受损。单核细胞增生。 M增强了先前存在的炎症，选择性地损害了复制免疫原的T细胞启动能力，使CD8 + T细胞对卵白蛋白作为一种惰性抗原（卵清蛋白-古人小体）的反应得以增强。 bovis BCG的预免疫，而卵白蛋白作为活体免疫原（单核细胞增生李斯特菌-卵清蛋白）的初免受到损害。因此，取决于免疫原的性质，先前炎症反应的存在可能会阻碍或提高疫苗效力。

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