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葡萄球菌肠毒素B会加重小鼠中由II型胶原蛋白诱导的关节炎的严重程度。

Staphylococcal enterotoxin B increases the severity of type II collagen induced arthritis in mice.

作者信息

Wooley P H, Cingel B

机构信息

Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan, USA.

出版信息

Ann Rheum Dis. 1995 Apr;54(4):298-304. doi: 10.1136/ard.54.4.298.

Abstract

OBJECTIVE

To observe the influence of T cell subset changes on the development of experimental arthritis, by using the bacterial superantigen staphylococcal enterotoxin B (SEB) to modulate the T cell repertoire during the arthritogenic response to type II collagen (CII) in vivo.

METHODS

DBA/1 mice were injected with SEB before immunisation with CII, and assessed for the development of collagen induced arthritis (CIA) and an immune response to CII. Mice with established arthritis were also treated therapeutically with SEB. Flow cytometry was used to evaluate the effect of the therapy on T cell subsets and T cell receptor (TCR) V beta expression.

RESULTS

Mice injected with SEB developed arthritis significantly faster than saline treated control animals, and developed more severe clinical features. Mice treated with SEB after the onset of CIA were also observed to progress more rapidly to a severe arthritis than mice treated with saline alone. The level of anti-CII antibody was not affected by SEB injection. Flow cytometric analysis of TCR expression in mice 21 days after injection of CII showed decreased expression of V beta 6 and V beta 8 cells in SEB treated mice, compared with collagen immunised control mice. Injection of SEB alone caused a decrease in V beta 8, but not V beta 6 T cells compared with the values in normal DBA/1 mice. No significant variations in the T cell repertoire were detected 70 days after CII immunisation.

CONCLUSIONS

Treatment with the bacterial enterotoxin SEB before the induction of arthritis did not suppress the immunological or arthritogenic response to CII in DBA/1 mice, despite the modulation of the V beta 8 T cell subset. Treatment of mice with established arthritis using SEB provoked a more severe disease course.

摘要

目的

通过使用细菌超抗原葡萄球菌肠毒素B(SEB)在体内对II型胶原蛋白(CII)的致关节炎反应过程中调节T细胞库,观察T细胞亚群变化对实验性关节炎发展的影响。

方法

DBA/1小鼠在免疫CII前注射SEB,并评估胶原诱导性关节炎(CIA)的发展及对CII的免疫反应。对已患关节炎的小鼠也用SEB进行治疗。采用流式细胞术评估该治疗对T细胞亚群和T细胞受体(TCR)Vβ表达的影响。

结果

注射SEB的小鼠患关节炎的速度明显快于生理盐水处理的对照动物,且出现更严重的临床症状。在CIA发病后用SEB治疗的小鼠也比仅用生理盐水治疗的小鼠更快发展为严重关节炎。抗CII抗体水平不受SEB注射的影响。注射CII后21天对小鼠TCR表达进行流式细胞术分析显示,与胶原免疫的对照小鼠相比,SEB处理的小鼠中Vβ6和Vβ8细胞的表达降低。与正常DBA/1小鼠的值相比,单独注射SEB导致Vβ8 T细胞减少,但Vβ6 T细胞未减少。CII免疫70天后未检测到T细胞库有明显变化。

结论

在关节炎诱导前用细菌肠毒素SEB治疗,尽管调节了Vβ8 T细胞亚群,但并未抑制DBA/1小鼠对CII的免疫或致关节炎反应。用SEB治疗已患关节炎的小鼠会引发更严重的病程。

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