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T 细胞共刺激分子:嗜酸性食管炎发病机制中的共犯?

T cell co-stimulatory molecules: a co-conspirator in the pathogenesis of eosinophilic esophagitis?

机构信息

Department of Pediatrics, Case Western Reserve University School of Medicine, 11000 Euclid Avenue, Cleveland, OH 44106, USA.

出版信息

Dig Dis Sci. 2013 Jun;58(6):1497-506. doi: 10.1007/s10620-013-2599-8. Epub 2013 Mar 2.

DOI:10.1007/s10620-013-2599-8
PMID:23456499
Abstract

Eosinophilic esophagitis (EoE) has become a common gastrointestinal disease. It is characterized by severe eosinophil infiltration in the esophagus. EoE is strongly associated with food allergy, asthma, atopic dermatitis, and other allergic diseases. T lymphocytes, especially Th2 cells, play an instrumental role in the development of allergic inflammation. Recent studies have shown that the ligation of co-stimulatory molecules contributes to the activation, differentiation, and proliferation of T cells. In this review, we will discuss the growing evidence of co-stimulatory molecules including OX40, Light, and HVEM in the pathogenesis of Th2-driven EoE. Our goal is to provide the rationale for the development of novel therapy therapies that target co-stimulatory molecules.

摘要

嗜酸粒细胞性食管炎 (EoE) 已成为一种常见的胃肠道疾病。其特征是食管内有严重的嗜酸性粒细胞浸润。EoE 与食物过敏、哮喘、特应性皮炎和其他过敏性疾病密切相关。T 淋巴细胞,特别是 Th2 细胞,在过敏炎症的发展中起着重要作用。最近的研究表明,共刺激分子的交联有助于 T 细胞的激活、分化和增殖。在这篇综述中,我们将讨论共刺激分子 OX40、Light 和 HVEM 在 Th2 驱动的 EoE 发病机制中的作用的新证据。我们的目标是为靶向共刺激分子的新型治疗方法的开发提供理论依据。

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T cell co-stimulatory molecules: a co-conspirator in the pathogenesis of eosinophilic esophagitis?T 细胞共刺激分子:嗜酸性食管炎发病机制中的共犯?
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Immunologic and pathologic characterization of a novel swine biomedical research model for eosinophilic esophagitis.一种用于嗜酸性食管炎的新型猪生物医学研究模型的免疫学和病理学特征
Front Allergy. 2022 Nov 14;3:1029184. doi: 10.3389/falgy.2022.1029184. eCollection 2022.
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Realigning the LIGHT signaling network to control dysregulated inflammation.调整 LIGHT 信号通路网络以控制失调的炎症反应。
J Exp Med. 2022 Jul 4;219(7). doi: 10.1084/jem.20220236. Epub 2022 May 23.
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Increased Production of LIGHT by T Cells in Eosinophilic Esophagitis Promotes Differentiation of Esophageal Fibroblasts Toward an Inflammatory Phenotype.

本文引用的文献

1
Markers of antigen presentation and activation on eosinophils and T cells in the esophageal tissue of patients with eosinophilic esophagitis.嗜酸性粒细胞食管炎患者食管组织中嗜酸性粒细胞和 T 细胞上的抗原呈递和激活标志物。
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嗜酸性粒细胞性食管炎中 T 细胞 LIGHT 的产生增加促进食管成纤维细胞向炎症表型分化。
Gastroenterology. 2020 Nov;159(5):1778-1792.e13. doi: 10.1053/j.gastro.2020.07.035. Epub 2020 Jul 23.
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Do We Know What Causes Eosinophilic Esophagitis? A Mechanistic Update.我们知道嗜酸性食管炎的病因吗?机制更新
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Abnormal interactions between perifollicular mast cells and CD8+ T-cells may contribute to the pathogenesis of alopecia areata.毛囊周围肥大细胞与CD8 + T细胞之间的异常相互作用可能导致斑秃的发病机制。
PLoS One. 2014 May 15;9(5):e94260. doi: 10.1371/journal.pone.0094260. eCollection 2014.
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The pathogenesis of eosinophilic esophagitis: beyond the eosinophil.嗜酸性粒细胞性食管炎的发病机制:超越嗜酸性粒细胞
Dig Dis Sci. 2013 Jun;58(6):1445-8. doi: 10.1007/s10620-013-2679-9. Epub 2013 Apr 27.
美国的食管嗜酸性粒细胞增多症的流行情况因气候带而异。
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4
Reslizumab in children and adolescents with eosinophilic esophagitis: results of a double-blind, randomized, placebo-controlled trial.瑞利珠单抗治疗儿童和青少年嗜酸性食管炎:一项双盲、随机、安慰剂对照试验的结果。
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The signaling networks of the herpesvirus entry mediator (TNFRSF14) in immune regulation.疱疹病毒进入介体(TNFRSF14)信号网络在免疫调节中的作用。
Immunol Rev. 2011 Nov;244(1):169-87. doi: 10.1111/j.1600-065X.2011.01064.x.
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Abrogation of CD30 and OX40 signals prevents autoimmune disease in FoxP3-deficient mice.阻断 CD30 和 OX40 信号可预防 FoxP3 缺陷型小鼠的自身免疫病。
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Differences in allergen-induced T cell activation between allergic asthma and rhinitis: Role of CD28, ICOS and CTLA-4.变应原诱导的 T 细胞活化在过敏性哮喘和鼻炎中的差异:CD28、ICOS 和 CTLA-4 的作用。
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