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豚鼠实验性自身免疫性肾小管间质性疾病发病机制的研究。IV. 硝唑咪未能抑制单核细胞聚集。

Studies on the pathogenesis of experimental autoimmune renal tubulointerstitial disease in guinea-pigs. IV. failure to inhibit mononuclear cell accumulation with niridazole.

作者信息

Rudofsky U H, Pollara B

出版信息

Clin Exp Immunol. 1977 Mar;27(3):522-5.

Abstract

Niridazole is a potent inhibitor of certain expressions of delayed-type hypersensitivity; however, its effect and specificity on other immunologically induced mononuclear cell infiltrates has not been determined. We therefore tested this drug in a model of auto-antibody-induced renal tubulointerstitial disease (RTD), which is characterized by the accumulation of lymphocytes and macrophages in the cortical interstitium. Niridazole-treated (100 mg/kg) and untreated guineapigs were injected with potent anti-tubular basement membrane serum from donors with RTD. Drug treatment was repeated 2-3 times during the course of 10 days. The characteristic renal lesions were found in both groups. However, a single dose of niridazole inhibited skin reactivity in tuberculin sensitive guinea-pigs for at least 8 days. These findings further support the contention that immunologic tissue injury in RTD does not involve mechanisms of delayed-type hypersensitivity.

摘要

硝唑咪是迟发型超敏反应某些表现的有效抑制剂;然而,其对其他免疫诱导的单核细胞浸润的作用和特异性尚未确定。因此,我们在自身抗体诱导的肾小管间质性疾病(RTD)模型中测试了这种药物,该疾病的特征是淋巴细胞和巨噬细胞在皮质间质中积聚。给硝唑咪治疗组(100mg/kg)和未治疗的豚鼠注射来自患有RTD的供体的强效抗肾小管基底膜血清。在10天的过程中重复给药2 - 3次。两组均发现了特征性的肾脏病变。然而,单剂量的硝唑咪至少8天抑制了结核菌素敏感豚鼠的皮肤反应性。这些发现进一步支持了RTD中的免疫组织损伤不涉及迟发型超敏反应机制的观点。

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