IL-13 released by and localized in human basophils.

IL-13 released by and localized in human basophils.
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DOI:
10.4049/jimmunol.156.12.4833
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发表时间:
1996-06
影响因子:
4.4
通讯作者:
Huamin Li;Tommy C. Sim;Rafeul Alam
Huamin Li;Tommy C. Sim;Rafeul Alam
中科院分区:
医学2区
文献类型:
--
作者:
Huamin Li;Tommy C. Sim;Rafeul Alam

文献摘要

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我们和其他人已经证明人类嗜碱性粒细胞可以合成和释放 IL-4。然而,IL-13(一种与 IL-4 非常相似的细胞因子)迄今尚未被描述为嗜碱性粒细胞产物。免疫细胞化学证明嗜碱性粒细胞产生 IL-13。大约 70% 的嗜碱性粒细胞经抗 FcepsilonRIalpha(IgE 受体 I 型 α 亚基的抗体)刺激后会出现 IL-13 染色。在类似的实验条件下,单核细胞未能对 IL-13 进行染色。通过免疫金染色的电子显微镜检查,细胞因子定位于嗜碱性颗粒。通过ELISA测定培养物上清液中IL-13的分泌。动力学研究显示 3 小时可检测到 IL-13 释放,并稳定增加直至 24 小时。这与嗜碱性粒细胞组胺和 IL-4 释放的动力学显着不同。在用抗IgE、抗FcepsilonRIα、IL-3和A23187以剂量依赖性方式刺激后,还观察到IL-13的产生。从同一供体分离的 PBMC、中性粒细胞和嗜酸性粒细胞在抗 IgE 刺激后不释放 IL-13。 IL-3预孵育可以增强抗IgE诱导的嗜碱性粒细胞IL-13合成(有和没有IL-3预孵育,抗IgE诱导的IL-13产量分别为227 +/- 99和42 +/- 13 pg/10(6)嗜碱性粒细胞)。 PBMC 在用 PHA 刺激后产生大量的 IL-1 3 ,但响应 A23187 和/或 PMA 产生低水平的 IL-13 。当与 A23187、IL-5 和抗 FcepsilonRIalpha 一起培养时,嗜酸性粒细胞和中性粒细胞不产生 IL-13。这是嗜碱性粒细胞产生 IL-1 3 的首次演示。我们的数据表明,嗜碱性粒细胞除了分泌介质之外,还可以代表促过敏细胞因子的重要来源。
We and others have shown that human basophils can synthesize and release IL-4. However, IL-13, a cytokine that closely resembles IL-4, has not hitherto been described as a basophil product. The production of IL-13 by basophils was demonstrated by immunocytochemistry. Approximately 70% of basophils stimulated with anti-FcepsilonRIalpha (antibody to the alpha subunit of IgE receptor type I) stained for IL-13. Under similar experimental conditions, mononuclear cells failed to stain for IL-13. The cytokine was localized to basophilic granules by electron microscopic examination of immunogold staining. The secretion of IL-13 into the culture supernatant was assayed by ELISA. Kinetic studies showed detectable IL-13 release at 3 h, which steadily increased up to 24 h. This is significantly different from the kinetics of basophil histamine and IL-4 release. IL-13 production was also observed upon stimulation with anti-IgE, anti-FcepsilonRIalpha, IL-3, and A23187 in a dose-dependent manner. PBMC, neutrophils, and eosinophils isolated from the same donors did not release IL-13 after anti-IgE stimulation. The anti-IgE-induced basophil IL-13 synthesis could be enhanced by IL-3 preincubation (with and without IL-3 preincubation, anti-IgE-induced IL-13 production was 227 +/- 99 and 42 +/- 13 pg/10(6) basophils, respectively). PBMC produced a significant amount of IL-1 3 upon stimulation with PHA, but a low level of IL-13 in response to A23187 and/or PMA. Eosinophils and neutrophils did not produce IL-13 when cultured with A23187, IL-5, and anti-FcepsilonRIalpha. This is the first demonstration of IL-1 3 production by basophils. Our data suggest that basophils, in addition to secreting mediators, can represent an important source of proallergic cytokines.