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莱姆关节炎中的辅助性T细胞反应:治疗抵抗性或治疗反应性莱姆关节炎患者对伯氏疏螺旋体外膜蛋白A的差异识别

The T helper cell response in Lyme arthritis: differential recognition of Borrelia burgdorferi outer surface protein A in patients with treatment-resistant or treatment-responsive Lyme arthritis.

作者信息

Lengl-Janssen B, Strauss A F, Steere A C, Kamradt T

机构信息

Department of Medicine, New England Medical Center Hospitals, Tufts University School of Medicine, Boston, Massachusetts 02111.

出版信息

J Exp Med. 1994 Dec 1;180(6):2069-78. doi: 10.1084/jem.180.6.2069.

Abstract

The host response to Borrelia burgdorferi is likely to play a role in the pathogenesis of Lyme arthritis. Whereas most patients with Lyme arthritis can be cured with antibiotic therapy, approximately 10% of the patients have persistent arthritis for months or even several years after antibiotic treatment. In this study, we tested the hypothesis that the T cell response to one or more antigens of B. burgdorferi is different in patients with treatment-responsive or treatment-resistant Lyme arthritis. For this purpose, 313 B. burgdorferi-specific T cell lines were derived from the synovial fluid or peripheral blood of four patients with treatment-responsive Lyme arthritis and five patients with treatment-resistant arthritis. 87 T cell lines from treatment-responsive Lyme arthritis and 112 lines from the treatment-resistant group were examined for the recognition of five recombinant. B. burgdorferi proteins: outer surface proteins A (OspA), B, C, p39, and p93. In both groups of patients, the T cell lines frequently recognized OspB, and only occasionally recognized OspC, p39, and p93. In contrast, OspA was preferentially recognized by T cell lines from patients with treatment-resistant arthritis, but only rarely recognized by T cell lines from patients with treatment-responsive arthritis (odds ratio 28.4, 95% confidence interval 9.2-87.8, p < 0.005). These results are compatible with the hypothesis that the T cell response to B. burgdorferi OspA is involved in the pathogenesis of treatment-resistant Lyme arthritis.

摘要

宿主对伯氏疏螺旋体的反应可能在莱姆关节炎的发病机制中起作用。虽然大多数莱姆关节炎患者可以通过抗生素治疗治愈,但约10%的患者在抗生素治疗后仍会持续数月甚至数年的关节炎。在本研究中,我们检验了这样一个假设:对伯氏疏螺旋体一种或多种抗原的T细胞反应在治疗反应性或治疗抵抗性莱姆关节炎患者中有所不同。为此,从4例治疗反应性莱姆关节炎患者和5例治疗抵抗性关节炎患者的滑液或外周血中获得了313条伯氏疏螺旋体特异性T细胞系。对87条来自治疗反应性莱姆关节炎的T细胞系和112条来自治疗抵抗组的T细胞系进行检测,以观察它们对5种重组伯氏疏螺旋体蛋白的识别情况:外表面蛋白A(OspA)、B、C、p39和p93。在两组患者中,T细胞系经常识别OspB,而仅偶尔识别OspC、p39和p93。相比之下,OspA优先被治疗抵抗性关节炎患者的T细胞系识别,但很少被治疗反应性关节炎患者的T细胞系识别(优势比28.4,95%置信区间9.2 - 87.8,p < 0.005)。这些结果与以下假设相符:对伯氏疏螺旋体OspA的T细胞反应参与了治疗抵抗性莱姆关节炎的发病机制。

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本文引用的文献

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The biological and social phenomenon of Lyme disease.莱姆病的生物学和社会现象。
Science. 1993 Jun 11;260(5114):1610-6. doi: 10.1126/science.8503006.
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The persistence of spirochetal nucleic acids in active Lyme arthritis.活性莱姆关节炎中螺旋体核酸的持续存在。
Ann Intern Med. 1994 Mar 15;120(6):487-9. doi: 10.7326/0003-4819-120-6-199403150-00007.

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