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伯氏疏螺旋体特异性T淋巴细胞可引发严重的破坏性莱姆关节炎。

Borrelia burgdorferi-specific T lymphocytes induce severe destructive Lyme arthritis.

作者信息

Lim L C, England D M, DuChateau B K, Glowacki N J, Schell R F

机构信息

Wisconsin State Laboratory of Hygiene, University of Wisconsin, Madison 53706.

出版信息

Infect Immun. 1995 Apr;63(4):1400-8. doi: 10.1128/iai.63.4.1400-1408.1995.

Abstract

This is the first documentation that Borrelia burgdorferi-specific T lymphocytes are involved in the pathogenesis of Lyme arthritis. We present direct evidence that T lymphocytes obtained from inbred LSH hamsters vaccinated with a whole-cell preparation of Formalin-inactivated B. burgdorferi sensu stricto isolate C-1-11 in adjuvant conferred on naive recipient hamsters the ability to develop severe destructive arthritis when challenged with B. burgdorferi sensu stricto isolates C-1-11 and 297. By contrast, recipients infused with normal T lymphocytes and challenged with B. burgdorferi sensu stricto isolates C-1-11 and 297 failed to develop severe destructive arthritis. The T lymphocytes transferred were obtained from the lymph nodes of vaccinated and nonvaccinated hamsters by depleting B lymphocytes by using monoclonal antibody 14-4-4s (< 1% B lymphocytes by flow cytometric analysis). The enriched T lymphocytes showed enhanced proliferation to stimulation with concanavalin A and failed to respond to lipopolysaccharide. Moreover, only the enriched T lymphocytes from vaccinated hamsters proliferated on exposure to a whole-cell preparation of B. burgdorferi sensu stricto isolate C-1-11 in the presence of mitomycin-treated syngeneic antigen-presenting cells. These results demonstrate that B. burgdorferi-specific T lymphocytes primed by vaccination with a whole-cell preparation of inactivated B. burgdorferi sensu stricto isolate C-1-11 in adjuvant are involved in the development of severe destructive arthritis. Additional experiments are needed to define the precise mechanism(s) responsible for the development of Lyme arthritis.

摘要

这是关于伯氏疏螺旋体特异性T淋巴细胞参与莱姆关节炎发病机制的首次文献记载。我们提供了直接证据,即从用福尔马林灭活的伯氏疏螺旋体狭义种C-1-11全细胞制剂加佐剂免疫的近交系LSH仓鼠中获得的T淋巴细胞,在给未免疫的受体仓鼠接种伯氏疏螺旋体狭义种C-1-11和297后,赋予了它们发生严重破坏性关节炎的能力。相比之下,输注正常T淋巴细胞并接种伯氏疏螺旋体狭义种C-1-11和297的受体仓鼠未发生严重破坏性关节炎。转移的T淋巴细胞是通过使用单克隆抗体14-4-4s清除B淋巴细胞(通过流式细胞术分析B淋巴细胞<1%),从免疫和未免疫仓鼠的淋巴结中获得的。富集的T淋巴细胞对刀豆球蛋白A刺激的增殖增强,对脂多糖无反应。此外,只有来自免疫仓鼠的富集T淋巴细胞在丝裂霉素处理的同基因抗原呈递细胞存在的情况下,接触伯氏疏螺旋体狭义种C-1-11全细胞制剂时才会增殖。这些结果表明,用福尔马林灭活的伯氏疏螺旋体狭义种C-1-11全细胞制剂加佐剂免疫引发的伯氏疏螺旋体特异性T淋巴细胞参与了严重破坏性关节炎的发展。需要进一步的实验来确定导致莱姆关节炎发展的确切机制。

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