Suppr超能文献

低剂量电离辐射对激活的大鼠嗜碱性白血病(RBL-2H3)肥大细胞的影响。

The effects of low-dose ionizing radiation in the activated rat basophilic leukemia (RBL-2H3) mast cells.

机构信息

Radiation Effect Research Team, Radiation Health Research Institute, Korea Hydro and Nuclear Power Co., Ltd., Seoul 132-703, Korea.

出版信息

J Biol Chem. 2012 Aug 10;287(33):27789-95. doi: 10.1074/jbc.M112.378497. Epub 2012 Jun 14.

Abstract

Mast cells play important roles in many biological responses, such as those during allergic diseases and inflammatory disorders. Although laser and UV irradiation have immunosuppressive effects on inflammatory diseases by suppressing mast cells, little is known about the effects of γ-ionizing radiation on mast cells. In this study, we investigated the effects of γ-ionizing radiation on RBL-2H3 cells, a convenient model system for studying regulated secretion by mast cells. Low-dose radiation (<0.1 gray (Gy)) did not induce cell death, but high-dose radiation (>0.5 Gy) induced apoptosis. Low-dose ionizing radiation significantly suppressed the release of mediators (histamine, β-hexosaminidase, IL-4, and tumor necrosis factor-α) from immunoglobulin E (IgE)-sensitized RBL-2H3 cells. To determine the mechanism of mediator release inhibition by ionizing radiation, we examined the activation of intracellular signaling molecules such as Lyn, Syk, phospholipase Cγ, PKCs, and MAPK, and intracellular free calcium concentrations (Ca(2+)). The phosphorylation of signaling molecules following stimulation of high-affinity IgE receptor I (FcεRI) was specifically inhibited by low-dose ionizing radiation (0.01 Gy). These results were due to the suppression of FcεRI expression by the low-dose ionizing radiation. Therefore, low-dose ionizing radiation (0.01 Gy) may function as a novel inhibitor of mast cell activation.

摘要

肥大细胞在许多生物学反应中发挥重要作用,如过敏疾病和炎症性疾病期间。尽管激光和紫外线照射通过抑制肥大细胞对炎症性疾病具有免疫抑制作用,但对γ-电离辐射对肥大细胞的影响知之甚少。在这项研究中,我们研究了γ-电离辐射对 RBL-2H3 细胞的影响,RBL-2H3 细胞是研究肥大细胞调节分泌的便利模型系统。低剂量辐射(<0.1 戈瑞(Gy))不会诱导细胞死亡,但高剂量辐射(>0.5 Gy)会诱导细胞凋亡。低剂量电离辐射显著抑制免疫球蛋白 E(IgE)致敏的 RBL-2H3 细胞释放介质(组胺、β-己糖胺酶、IL-4 和肿瘤坏死因子-α)。为了确定电离辐射抑制介质释放的机制,我们检查了细胞内信号分子(如 Lyn、Syk、磷脂酶 Cγ、PKC 和 MAPK)和细胞内游离钙浓度([Ca(2+)](i))的激活。高亲和力 IgE 受体 I(FcεRI)刺激后信号分子的磷酸化被低剂量电离辐射(0.01 Gy)特异性抑制。这些结果归因于低剂量电离辐射对 FcεRI 表达的抑制。因此,低剂量电离辐射(0.01 Gy)可能作为肥大细胞活化的新型抑制剂发挥作用。

相似文献

引用本文的文献

本文引用的文献

1
Ubiquitination and endocytosis of the high affinity receptor for IgE.IgE 高亲和力受体的泛素化和内吞作用。
Mol Immunol. 2010 Sep;47(15):2427-34. doi: 10.1016/j.molimm.2010.06.003. Epub 2010 Jul 16.
6
The effect of chronic ultraviolet radiation on the human immune system.慢性紫外线辐射对人体免疫系统的影响。
Photochem Photobiol. 2008 Jan-Feb;84(1):19-28. doi: 10.1111/j.1751-1097.2007.00239.x.
9
The role of the mast cell in the pathophysiology of asthma.肥大细胞在哮喘病理生理学中的作用。
J Allergy Clin Immunol. 2006 Jun;117(6):1277-84. doi: 10.1016/j.jaci.2006.02.039. Epub 2006 Apr 27.
10
Ultraviolet immunosuppression: mechanisms and consequences.紫外线免疫抑制:机制与后果
Dermatol Clin. 2006 Jan;24(1):19-25. doi: 10.1016/j.det.2005.08.003.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验