淋巴因子与炎性白细胞间关节内反应在豚鼠关节炎的产生。

G A Limb, K A Brown, R A Wolstencroft, B A Ellis, D C Dumonde
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引用次数: 0

摘要

向豚鼠膝关节单次关节内注射淋巴因子导致关节结构的一系列变化,其组织病理学特征类似于急性炎症反应进展到慢性状态。24小时,滑膜轻度增生和肥大,伴有强烈的多形核白细胞浸润。72h时,滑膜大量浸润,单核细胞呈弥漫性和局灶性聚集;滑膜鞘对软骨和骨的侵蚀伴有滑膜下纤维化。1周时,滑膜白细胞浸润明显减少,但糜烂和纤维化持续存在。然而,当淋巴因子与油诱导的腹膜渗出细胞一起注射时,更严重的关节炎随之而来:72小时滑膜滑膜明显侵蚀骨,并伴有侵蚀区出现类似破骨细胞的多核细胞。这些特征被证明与豚鼠实验性过敏性关节炎的组织病理学非常相似,而由迟发性超敏反应的过继细胞转移到关节引起的滑膜炎的严重程度较轻。结果表明,淋巴因子可能通过招募和激活参与慢性炎症的细胞,在实验性过敏性关节炎的诱导中发挥作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The production of arthritis in the guinea-pig by intra-articular reaction between lymphokines and inflammatory leucocytes.

A single intra-articular injection of lymphokine into the guinea-pig knee joint resulted in a sequence of changes in joint architecture whose histopathological features resembled that of an acute inflammatory reaction progressing to a chronic state. At 24 h there was a mild hyperplasia and hypertrophy of the synovium with intense polymorphonuclear leucocyte infiltration. At 72 h, the synovium was heavily infiltrated with diffuse and focal aggregations of mononuclear cells; erosion of cartilage and bone by synovial pannus was accompanied by a subsynovial fibrosis. By 1 week, leucocytic infiltration of the synovium had decreased markedly although the erosion and fibrosis persisted. However, when lymphokine was injected together with oil-elicited peritoneal exudate cells a more intense arthritis ensued: at 72 h synovial pannus was prominently eroding bone and this was accompanied by the appearance of multinucleate cells resembling osteoclasts in the zone of erosion. These features were shown to resemble closely the histopathology of experimental allergic arthritis in the guinea-pig, in contrast to the lesser severity of synovitis resulting from the adoptive cellular transfer of delayed hypersensitivity into the joint. The results indicate that lymphokines may play a role in the induction of experimental allergic arthritis by recruiting and activating cells involved in chronic inflammation.

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