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在因胶原诱导性关节炎而受到抑制的小鼠中,抗II型胶原抗体亚型的表达受到限制。

Restricted expression of anti-type II collagen antibody isotypes in mice suppressed for collagen-induced arthritis.

作者信息

Kresina T F, Finegan C K

出版信息

Ann Rheum Dis. 1986 Jan;45(1):60-6. doi: 10.1136/ard.45.1.60.

Abstract

The present study details the time course and isotype distribution of the immune response to type II collagen in collagen-induced arthritic mice and mice suppressed for collagen-induced arthritis. The serum of arthritic mice was observed to contain significantly higher (p less than 0.005) concentrations of antibodies to type II collagen than that of mice suppressed for arthritis at all times tested. For the arthritic mice anti-type II collagen antibodies ranged from 0.2 +/- 0.2 (SD) to 6.1 +/- 0.7 mg/ml (g/l). Serum values for mice suppressed for arthritis ranged from 0.05 +/- 0.04 to 0.6 +/- 0.04 mg/ml. Analysis of the isotypes of these responses showed an expression of anticollagen molecules restricted to the IgG1 subclass in mice suppressed for collagen arthritis throughout the time course (p less than 0.01). The data indicate that mice suppressed for collagen-induced arthritis can mount a primary and secondary immune response to the arthrogenic stimuli. This response, however, is mainly restricted to the IgG1 subclass of antibodies. This restricted subclass expression of anticollagen antibodies may represent a mechanism of suppression of arthritis in the murine model of collagen-induced arthritis.

摘要

本研究详细阐述了胶原诱导性关节炎小鼠以及胶原诱导性关节炎受抑制小鼠对II型胶原免疫反应的时间进程和同种型分布。在所有测试时间点,观察到关节炎小鼠血清中抗II型胶原抗体的浓度显著高于关节炎受抑制小鼠(p<0.005)。对于关节炎小鼠,抗II型胶原抗体的浓度范围为0.2±0.2(标准差)至6.1±0.7mg/ml(g/l)。关节炎受抑制小鼠的血清值范围为0.05±0.04至0.6±0.04mg/ml。对这些反应的同种型分析表明,在整个时间进程中,胶原关节炎受抑制小鼠中抗胶原分子的表达仅限于IgG1亚类(p<0.01)。数据表明,胶原诱导性关节炎受抑制小鼠能够对致关节炎刺激产生初次和二次免疫反应。然而,这种反应主要限于抗体的IgG1亚类。抗胶原抗体这种受限的亚类表达可能代表了胶原诱导性关节炎小鼠模型中关节炎抑制的一种机制。

相似文献

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IgG subclasses in collagen-induced arthritis in the rat.
Immunol Lett. 1984;7(5):243-7. doi: 10.1016/0165-2478(84)90029-4.

本文引用的文献

4
IgG subclasses in collagen-induced arthritis in the rat.
Immunol Lett. 1984;7(5):243-7. doi: 10.1016/0165-2478(84)90029-4.

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