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点滴状银屑病患者外周血淋巴细胞对链球菌超抗原反应低下:由局部感染的化脓性链球菌释放的超抗原对T细胞进行全身刺激的证据。

Hyporesponsiveness of peripheral blood lymphocytes to streptococcal superantigens in patients with guttate psoriasis: evidence for systemic stimulation of T cells with superantigens released from focally infecting Streptococcus pyogenes.

作者信息

Tokura Y, Seo N, Ohshima A, Wakita H, Yokote R, Furukawa F, Takigawa M

机构信息

Department of Dermatology, Hamamatsu University School of Medicine, Japan.

出版信息

Arch Dermatol Res. 1999 Jul-Aug;291(7-8):382-9. doi: 10.1007/s004030050426.

DOI:10.1007/s004030050426
PMID:10482006
Abstract

Throat infection with Streptococcus pyogenes is the most important trigger for acute guttate psoriasis. We examined the in vitro responses of peripheral blood mononuclear cells (PBMC) to streptococcal superantigens, SPEA and SPEC, and staphylococcal superantigens, SEB and TSST-1, in patients with guttate psoriasis, in patients with chronic plaque psoriasis, and in healthy subjects. PBMC from patients with guttate psoriasis responded poorly to SPEA and SPEC at concentrations of 0.1 and 1 ng/ml as compared with those from patients with plaque psoriasis, but showed high responses to SEB and TSST-1. The hyporesponsiveness recovered after improvement of the skin eruption. There was no significant difference between guttate and chronic types of psoriasis in the percentage of circulating T-cell receptor BV2 or BV8-bearing T cells, responsive to streptococcal superantigens, indicating that T-cell clonal anergy was a mechanism underlying the hyporesponsiveness. Our results suggest that superantigens released from focally infecting S. pyogenes induce a transient activation of relevant T cells, leading to the development of skin eruption and, subsequently, temporary T-cell anergy to these toxins.

摘要

化脓性链球菌引起的咽喉感染是急性点滴状银屑病最重要的触发因素。我们检测了点滴状银屑病患者、慢性斑块状银屑病患者和健康受试者外周血单个核细胞(PBMC)对链球菌超抗原SPEA和SPEC以及葡萄球菌超抗原SEB和TSST-1的体外反应。与斑块状银屑病患者相比,点滴状银屑病患者的PBMC在0.1和1 ng/ml浓度下对SPEA和SPEC反应较差,但对SEB和TSST-1反应较高。皮肤疹改善后,低反应性恢复。在对链球菌超抗原产生反应的循环T细胞受体BV2或BV8阳性T细胞百分比方面,点滴状银屑病和慢性银屑病类型之间没有显著差异,这表明T细胞克隆无能是低反应性的潜在机制。我们的结果表明,局部感染的化脓性链球菌释放的超抗原诱导相关T细胞的短暂激活,导致皮疹的出现,随后对这些毒素产生暂时的T细胞无能。

相似文献

1
Hyporesponsiveness of peripheral blood lymphocytes to streptococcal superantigens in patients with guttate psoriasis: evidence for systemic stimulation of T cells with superantigens released from focally infecting Streptococcus pyogenes.点滴状银屑病患者外周血淋巴细胞对链球菌超抗原反应低下:由局部感染的化脓性链球菌释放的超抗原对T细胞进行全身刺激的证据。
Arch Dermatol Res. 1999 Jul-Aug;291(7-8):382-9. doi: 10.1007/s004030050426.
2
Peripheral blood lymphocytes from psoriatic patients are hyporesponsive to beta-streptococcal superantigens.银屑病患者的外周血淋巴细胞对β-链球菌超抗原反应低下。
Br J Dermatol. 1998 Feb;138(2):229-35. doi: 10.1046/j.1365-2133.1998.02066.x.
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Evidence for a streptococcal superantigen-driven process in acute guttate psoriasis.急性点滴状银屑病中链球菌超抗原驱动过程的证据。
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Decreased IL-10 production by psoriatic peripheral blood mononuclear cells stimulated with streptococcal superantigen.用链球菌超抗原刺激的银屑病外周血单个核细胞产生白细胞介素-10减少。
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Streptococcal superantigen-induced expansion of human tonsil T cells leads to altered T follicular helper cell phenotype, B cell death and reduced immunoglobulin release.链球菌超抗原诱导的人扁桃体 T 细胞扩增导致 T 滤泡辅助细胞表型改变、B 细胞死亡和免疫球蛋白释放减少。
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