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嗜酸性粒细胞增多症VI,哮喘性支气管炎患者支气管T淋巴细胞对嗜酸性粒细胞的趋化动力学、趋化性、补体受体诱导活性的自发合成。

Eosinophilia VI, spontaneous synthesis of chemokinetics, chemotactic, complement receptor-inducing activities for eosinophils by bronchial t lymphocytes of asthmatic-bronchitic patients.

作者信息

Parish W E, Luckhurst E

出版信息

Clin Allergy. 1982 Sep;12(5):475-88. doi: 10.1111/j.1365-2222.1982.tb01646.x.

Abstract

T lymphocytes were separated from the bronchial mucus of five patients with extrinsic asthma and chronic and mild bronchitis and who had numerous eosinophils in the bronchial mucus but no significant blood eosinophilia. The bronchial lymphocytes spontaneously, that is without treatment with antigens or mitogens, released into serum-free synthetic medium one or more substances in the molecular weight range of 30 000 to 60 000 daltons. These substances when tested on eosinophils of normal persons stimulated random movement (chemokinesis), attracted them (chemotaxis), enhanced their chemotactic response to activated complement, and increased the expression of C4 and C3b receptors. Chemokinetic and chemotactic activity for neutrophils was weak. No eosinophil-stimulating activity was found in cultures of bronchial lymphocytes treated with puromycin to inhibit synthesis. The blood lymphocytes did not spontaneously synthesize the substance(s). It is not known if the several eosinophil-stimulating activities are due to one or more substance(s), but the nature of the eosinophil responses, molecular weight and other features, indicate similarities with the 'eosinophil stimulation promoter-chemotactic' factor reported to be released from mouse or human lymphocytes treated with antigen. Eosinophil stimulation resulting in increased expression of specific receptors, and potential for non-specific adherence, by trapping or arresting randomly migrating cells, is believed to mediate accumulation of cells in an affected organ. Prolonged synthesis of such products as from activated lymphocytes in the lung, could account for much of the local eosinophilia.

摘要

从5例患有外源性哮喘、慢性轻度支气管炎且支气管黏液中有大量嗜酸性粒细胞但血液嗜酸性粒细胞无明显增多的患者的支气管黏液中分离出T淋巴细胞。这些支气管淋巴细胞在未用抗原或有丝分裂原处理的情况下,即自发地向无血清合成培养基中释放出一种或多种分子量在30000至60000道尔顿范围内的物质。这些物质在对正常人的嗜酸性粒细胞进行测试时,可刺激其随机运动(化学增活作用)、吸引它们(趋化作用)、增强它们对活化补体的趋化反应,并增加C4和C3b受体的表达。对中性粒细胞的化学增活和趋化活性较弱。在用嘌呤霉素处理以抑制合成的支气管淋巴细胞培养物中未发现嗜酸性粒细胞刺激活性。血液淋巴细胞不会自发合成该物质。尚不清楚几种嗜酸性粒细胞刺激活性是由一种还是多种物质引起的,但嗜酸性粒细胞反应的性质、分子量和其他特征表明,与报道的经抗原处理的小鼠或人淋巴细胞释放的“嗜酸性粒细胞刺激促进剂 - 趋化”因子相似。嗜酸性粒细胞刺激导致特异性受体表达增加,并通过捕获或阻止随机迁移的细胞而具有非特异性黏附的潜力,据信这介导了细胞在受影响器官中的积聚。肺部活化淋巴细胞等此类产物的持续合成可能是局部嗜酸性粒细胞增多的主要原因。

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