Immunological aspects of polymyositis. The in vitro activity of lymphocytes on incubation with muscle antigen and with muscle cultures.

Immunological aspects of polymyositis. The in vitro activity of lymphocytes on incubation with muscle antigen and with muscle cultures.
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多发性肌炎的免疫学方面。

DOI:
10.1093/oxfordjournals.qjmed.a067260
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发表时间:
1971
期刊:
The Quarterly journal of medicine
影响因子:
--
通讯作者:
Aileen E. Brown
Aileen E. Brown
中科院分区:
--
文献类型:
--
作者:
S. Currie;M. Saunders;M. Knowles;Aileen E. Brown

文献摘要

被引文献

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多发性肌炎是一种获得性肌病,分为三种类型:α型“无并发症”多发性肌炎; β型,皮肌炎和与结缔组织疾病相关的多发性肌炎; γ型,与瘤形成相关的多发性肌炎。这种疾病可能是由于淋巴细胞介导的超敏反应,因此研究了这种疾病患者淋巴细胞的体外活性。通过测量这些淋巴细胞对氚化胸苷的摄取,评估了这些淋巴细胞与全肌匀浆孵育时的刺激程度。多发性肌炎患者的淋巴细胞对肌肉的反应明显高于其他疾病伴或不伴肌肉萎缩患者的淋巴细胞。在多发性肌炎的反应指数表现出一定的相关性与临床活动的障碍。淋巴细胞从没有组的患者对其他抗原(胶原蛋白,致脑炎因子,肝脏和肾脏)。淋巴细胞的细胞毒活性已通过与培养物中的胎儿肌肉和其他组织一起孵育进行了研究。多发性肌炎患者的淋巴细胞对肌肉培养物具有细胞毒性;这些患者的血清和其他疾病患者的淋巴细胞无细胞毒性。来自α型(“无并发症”)多发性肌炎患者的淋巴细胞对成纤维细胞和上皮细胞培养物无细胞毒性,但来自γ型多发性肌炎患者的淋巴细胞则有细胞毒性。抗淋巴细胞抗血清似乎可以防止淋巴细胞的细胞毒性作用。肌肉抗原对淋巴细胞的刺激程度与淋巴细胞对肌肉培养物的细胞毒活性之间存在一定的相关性。在一个附属项目中,研究了系统性硬化症患者的淋巴细胞。这些淋巴细胞表现出提高指数的肌肉抗原的反应,只有当有肌病的临床证据,然而,淋巴细胞从所有患者的细胞毒性培养的所有tissues.The证据免疫发病机制在多发性肌炎和本研究结果的意义进行了讨论。肌肉抗原对淋巴细胞的刺激和对肌肉细胞的细胞毒活性似乎是特异性的。他们表明肌肉的某些成分已经发生了体内致敏作用。淋巴细胞刺激可能反映了继发性现象。体外细胞毒性与体内产生过敏性病变的相关性尚不确定。然而,研究结果表明,淋巴细胞可能有助于多发性肌炎的产生。根据我们的研究结果,对多发性肌炎的分类进行了综述。雷诺现象、关节痛和红斑可能并不总是代表β型多发性肌炎的多系统受累。
Polymyositis is an acquired myopathy which is classified into three types: Type α ‘uncomplicated’ polymyositis; Type β, dermatomyositis and polymyositis associated with connective-tissue disorders; Type γ, polymyositis associated with neoplasia. The disorder may be due to lymphocyte-mediated hypersensitivity; thein vitroactivity of lymphocytes from patients with the condition has therefore been studied. The degree of stimulation of these lymphocytes on incubation with whole muscle homogenate has been assessed by measuring their uptake of tritiated thymidine. Lymphocytes from patients with polymyositis showed a significantly higher response to muscle than did lymphocytes from patients with other diseases with and without muscle wasting. In polymyositis the index of response showed some correlation with the clinical activity of the disorder. Lymphocytes from none of the groups of patients responded to other antigens (collagen, encephalitogenic factor, liver, and kidney). The cytotoxic activity of lymphocytes has been studied by incubation with foetal muscle and other tissues in culture. Lymphocytes from patients with polymyositis appeared to be cytotoxic to muscle cultures; serum from these patients and lymphocytes from those with other disorders were not cytotoxic. Lymphocytes from patients with Type α (‘uncomplicated’) polymyositis were not cytotoxic to fibroblast and epithelial cultures but lymphocytes from those with Type γ polymyositis were so. Antilymphocytic antiserum appeared to prevent cytotoxic action by lymphocytes. There was some correlation between the degree of lymphocytic stimulation by muscle antigen and the cytotoxic activity of lymphocytes against muscle cultures. In a subsidiary project lymphocytes from patients with systemic sclerosis were studied. These lymphocytes showed a raised index of response to muscle antigen only when there was clinical evidence of myopathy; however, lymphocytes from all the patients were cytotoxic to cultures of all tissues.The evidence for an immunological pathogenesis in polymyositis is given and the significance of the present findings is discussed. The lymphocytic stimulation by muscle antigen and the cytotoxic activity against muscle cells appear to be specific. They suggest thatin vivosensitization has occurred to some component of muscle. Lymphocytic stimulation may reflect a secondary phenomenon. The relevance of in vitro cytotoxicity to thein vivoproduction of hypersensitivity lesions is uncertain. However, the findings taken together suggest that lymphocytes may be instrumental in the production of polymyositis. The classification of polymyositis is reviewed in the light of our results. Raynaud's phenomenon, arthralgia, and erythema may not always represent the multi-system involvement of Type β polymyositis.