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通过原位杂交测量健康个体和免疫球蛋白缺陷患者中产生白细胞介素-5 mRNA的细胞频率。

Frequencies of interleukin-5 mRNA-producing cells in healthy individuals and in immunoglobulin-deficient patients, measured by in situ hybridization.

作者信息

Smith C I, Möller G, Severinson E, Hammarström L

机构信息

Department of Clinical Immunology, NOVUM, Karolinska Institute, Huddinge Hospital, Sweden.

出版信息

Clin Exp Immunol. 1990 Sep;81(3):417-22. doi: 10.1111/j.1365-2249.1990.tb05349.x.

DOI:10.1111/j.1365-2249.1990.tb05349.x
PMID:2397611
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1534998/
Abstract

Interleukin-5 (IL-5) has previously been demonstrated to enhance immunoglobulin synthesis, especially IgA. Thus, it could be hypothesized that a defect production of IL-5 may cause immunoglobulin deficiency. We have analysed the frequency of IL-5 mRNA-producing cells in healthy adults and in patients with common variable immunodeficiency or selective IgA deficiency. Unstimulated lymphocytes were rarely found to synthesize IL-5 as measured by in situ hybridization. However, pokeweed mitogen and several other activating ligands induced the synthesis of IL-5 mRNA in peripheral blood and spleen lymphocyte cultures. After pokeweed mitogen activation, the number of IL-5 mRNA-producing cells most often peaked on day 3 with a maximal frequency of around 1-2% of mononuclear cells. In a kinetic study we were unable to detect any peak frequency differences between healthy controls (mean 0.44%) and 20 patients (mean 0.58%). Thus, although IL-5 has been reported to be an important regulator of IgA synthesis, a defect production does not seem to be the underlying mechanism in human immunoglobulin deficiency.

摘要

白细胞介素-5(IL-5)先前已被证明可增强免疫球蛋白的合成,尤其是IgA。因此,可以推测IL-5产生缺陷可能导致免疫球蛋白缺乏。我们分析了健康成年人以及常见可变免疫缺陷或选择性IgA缺乏患者中产生IL-5 mRNA的细胞频率。通过原位杂交检测发现,未受刺激的淋巴细胞很少合成IL-5。然而,商陆有丝分裂原和其他几种激活配体可诱导外周血和脾淋巴细胞培养物中IL-5 mRNA的合成。经商陆有丝分裂原激活后,产生IL-5 mRNA的细胞数量通常在第3天达到峰值,最大频率约为单核细胞的1-2%。在一项动力学研究中,我们未能检测到健康对照组(平均0.44%)和20名患者(平均0.58%)之间在峰值频率上有任何差异。因此,尽管有报道称IL-5是IgA合成的重要调节因子,但产生缺陷似乎并不是人类免疫球蛋白缺乏的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/196d/1534998/71b258af90e3/clinexpimmunol00072-0065-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/196d/1534998/71b258af90e3/clinexpimmunol00072-0065-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/196d/1534998/71b258af90e3/clinexpimmunol00072-0065-a.jpg

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