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在注射弗氏佐剂的关节炎易感和不易感品系大鼠中,自体混合淋巴细胞反应降低。

The autologous mixed lymphocyte reaction is decreased in Freund's adjuvant-injected rats of arthritis-susceptible and -insusceptible strains.

作者信息

Crowe W E, Battisto J R, Smith R N

出版信息

Arthritis Rheum. 1985 May;28(5):537-41. doi: 10.1002/art.1780280512.

Abstract

We examined the T-non-T cell autologous mixed lymphocyte reaction (AMLR) of spleen cells from rats with arthritis induced by Freund's complete adjuvant in an effort to establish an animal model for the study of the relationship between the AMLR and autoimmune disease. We found that the splenic T-non-T AMLR was markedly decreased in rats with adjuvant-induced arthritis and that this decrease was mediated by suppressor cells within the nylon-wool-adherent stimulator cell population. However, we also found a similar decrease in the AMLR of arthritis-resistant Fisher 344 rats that received Freund's complete adjuvant but did not develop arthritis. Control animals with local inflammation induced by turpentine, a non-arthritogenic inflammatory substance, had normal AMLR, whereas other controls given Freund's incomplete adjuvant, also a non-arthritogenic substance, had a modest responder cell-mediated decrease in AMLR. These studies help to clarify the relationship between the decreased AMLR and the pathogenesis of adjuvant-induced arthritis by demonstrating that: 1) the acute-phase inflammatory response does not reduce the AMLR; and 2) the decreased AMLR can occur in the absence of overt autoimmune disease. This latter observation calls into question the proposed pathogenetic relationship between the AMLR and autoimmune disease states.

摘要

我们检测了弗氏完全佐剂诱导的关节炎大鼠脾脏细胞的T非T细胞自体混合淋巴细胞反应(AMLR),旨在建立一个动物模型来研究AMLR与自身免疫性疾病之间的关系。我们发现,佐剂诱导的关节炎大鼠的脾脏T非T AMLR显著降低,且这种降低是由尼龙毛黏附刺激细胞群体中的抑制细胞介导的。然而,我们还发现,接受弗氏完全佐剂但未发生关节炎的抗关节炎费希尔344大鼠的AMLR也有类似降低。用松节油(一种非致关节炎的炎性物质)诱导局部炎症的对照动物的AMLR正常,而给予弗氏不完全佐剂(也是一种非致关节炎物质)的其他对照动物的AMLR则有适度的反应细胞介导的降低。这些研究通过证明以下几点,有助于阐明AMLR降低与佐剂诱导的关节炎发病机制之间的关系:1)急性期炎症反应不会降低AMLR;2)在无明显自身免疫性疾病的情况下,AMLR也会降低。后一观察结果对AMLR与自身免疫性疾病状态之间提出的发病机制关系提出了质疑。

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